Food and Chemical Toxicology 86 (2015) 144153

Contents lists available at ScienceDirect

Food and Chemical Toxicology

journal homepage: www.elsevier.com/locate/foodchemtox

Review

Human dietary exposure to polycyclic aromatic hydrocarbons: A

review of the scientic literature
Jos L. Domingo, Mart Nadal
Laboratory of Toxicology and Environmental Health, School of Medicine, IISPV, Universitat Rovira i Virgili, Sant Lloren 21, 43201 Reus, Catalonia, Spain

a r t i c l e i n f o a b s t r a c t

Article history: Polycyclic aromatic hydrocarbons (PAHs) are a group of over 200 different organic compounds that
Received 11 August 2015 are mainly formed as the result of pyrolytic processes. For the general population, a number of stud-
Received in revised form 3 October 2015
ies have shown that, as for other environmental organic contaminants, the major route of exposure
Accepted 5 October 2015
to PAHs is through food consumption. In this paper, the scientic literature concerning the concentra-
Available online 9 October 2015
tions of PAHs in food and the human dietary intake of these compounds, is reviewed. Unexpectedly,
Keywords: we have detected a considerable lack of scientic papers for countries such as Australia, Canada, Ger-
Polycyclic aromatic hydrocarbons (PAHs) many, or Japan, among many others, which seems rather unusual given the important scientic and
Foodstuffs social interest on the knowledge of the health risks of human exposure to environmental pollutants.
Dietary intake The data from countries for which the human dietary intake of PAHs is available, show important dif-
Cooking procedures ferences among them, which would be explained by a number of factors, being probably the most im-
Health risks
portant, the different methodologies used in the respective surveys. Regarding the inuence of cooking
on the levels of PAHs in foodstuffs, and the consequent intake, we conclude that it depends, not only
on the particular cooking process, but even more on the specic characteristics of the respective food
items.
2015 Elsevier Ltd. All rights reserved.

Contents

1. Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ....... . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 145

2. Food and PAHs: dietary exposure in a number of countries. . . . . . . . . . . . . . . . . . ....... . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 145
2.1. European countries. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ....... . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 146
2.1.1. Spain. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ....... . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 146
2.1.2. Italy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ....... . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 148
2.1.3. The Netherlands . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ....... . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 148
2.1.4. United Kingdom . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ....... . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 148
2.1.5. Other European countries; Azerbaijan, Estonia, France, Greece and Sweden . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 149
2.2. Asia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ....... . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 149
2.2.1. China . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ....... . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 149
2.2.2. Korea . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ....... . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 150
2.2.3. India . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ....... . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 150
2.3. America . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ....... . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 150
2.3.1. USA. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ....... . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 150
2.3.2. Brazil . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ....... . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 151
2.4. Africa . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ....... . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 151
3. Inuence of cooking procedures on the concentrations of PAHs in food. . . . . . . . ....... . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 151
4. Summary and conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ....... . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 151
Conict of interest . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ....... . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 152

Corresponding author.
E-mail address: joseluis.domingo@urv.cat (J.L. Domingo).

http://dx.doi.org/10.1016/j.fct.2015.10.002
0278-6915/ 2015 Elsevier Ltd. All rights reserved.
 J.L. Domingo, M. Nadal / Food and Chemical Toxicology 86 (2015) 144153
Transparency document . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 152
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 152
1. Introduction
Polycyclic aromatic hydrocarbons (PAHs) are a group of over
200 different organic compounds with two or more fused aromatic
rings. They are mainly formed as the result of pyrolytic processes,
especially the incomplete combustion of organic matter during a
number of different activities and industrial processes. Most PAHs
are very lipophilic, having low water solubility. PAHs may be de-
tected in air, water, soils and sediments, where they are usually
found as complex mixtures (ATSDR, 2014).
For non-smokers and non-occupationally exposed individuals,
the major route of exposure to PAHs is through food consumption
(Phillips, 1999; Benford et al., 2010; Harris et al., 2013; Ma and
Harrad, 2015). With respect to children exposure, dietary intake
is also a relevant pathway, as infant foods, including powder milk
formulae and cereals, are likely to contain PAHs and hydroxylated
metabolites (Rey-Salgueiro et al., 2009a). The presence of PAHs in
foodstuffs depends on the environmental levels of these pollutants,
as well as the physiological and ecological characteristics of the
food item (Guilln, 1994; Falc et al., 2003; Ramesh et al., 2004;
Simon et al., 2008; Martorell et al., 2010). The amounts of PAHs
coming from food intake depends also on the different ways of
cooking, as well as the potential food contamination, which can
originate from manufacturing and packaging materials (Domingo,
2011; Fasano et al., 2016; Martorell et al., 2010; Perell et al., 2009;
Rey-Salgueiro et al., 2008; Viegas et al., 2014). With respect to al-
coholic drinks, which can also contain these carcinogenic chemi-
cals, the way the tree raw material is toasted strongly inuences
PAH levels in alcoholic drinks (Garca-Falcn and Simal-Gndara,
2005).
In recent years, PAHs have been evaluated by the International
Program on Chemical Safety (IPCS), the Scientic Committee on
Food (SCF), and by the Joint FAO/WHO Expert Committee on Food
Additives (JECFA). The SCF concluded that the following 15 PAHs:
benz[a]anthracene, benzo[b]uoranthene, benzo[j]uoranthene,
benzo[k]uoranthene, benzo[ghi]perylene, benzo[a]pyrene,
chrysene, cyclopenta[cd]pyrene, dibenzo[a,h]anthracene,
dibenzo[a,e]pyrene, dibenzo[a,h]pyrene, dibenzo[a,i]pyrene,
dibenzo[a,l]pyrene, indeno[1,2,3-c,d]pyrene and 5-methylchrysene,
showed clear evidence of mutagenicity/genotoxicity in somatic
cells in experimental animals. Moreover, with the exception
of benzo[g,h,i]perylene, these compounds also showed carcino-
genicity in various types of bioassays in experimental animals
(EFSA, 2008). The SCF suggested using benzo[a]pyrene, which
is the most studied of the PAHs, as a marker of occurrence
and effect of the carcinogenic PAHs in food. In a re-evaluation
of the genotoxicity and carcinogenicity of PAHs performed by
the JECFA, it was concluded that 13 PAHs were clearly geno-
toxic and carcinogenic, as also indicated by the SCF, with only
two exceptions: benzo[ghi]perylene and cyclopenta[cd]pyrene.
The JECFA concluded that benzo[a]pyrene could be used as a
marker of exposure to genotoxic and carcinogenic PAHs, also
recommending to include benzo[c]uorene into future analy-
ses on its occurrence in food (EFSA, 2008). Previously, the US
Environmental Protection Agency (US EPA) had already classi-
ed benz[a]anthracene, benzo[a]pyrene, benzo[b]uoranthene,
chrysene, benzo[k]uoranthene, dibenzo[a,h]anthracene, and
indeno[1,2,3-c,d]pyrene as probable human carcinogens (group
B2) (US EPA, 2008), while the International Agency for Re-
145
search on Cancer (IARC) established that benz[a]anthracene
and benzo[a]pyrene were probable human carcinogens, being
benzo[b]uoranthene, benzo[j]uoranthene, benzo[k]uoranthene,
and indeno[1,2,3-c,d]pyrene possible human carcinogens (IARC,
2004).
The presence in food of environmental chemicals in general,
and that of PAHs in particular, is a matter of concern that requires
continuous monitoring. In relation to this, it is important to remark
that various PAHs are potentially carcinogenic. In recent years, a
number of epidemiological studies have shown that a large propor-
tion of human cancers are attributable, at least in part, to dietary
factors, including dietary exposure to PAHs (Harris et al., 2013; Kim
et al., 2013; Abid et al., 2014).
In the last two decades, some authors have reviewed the pres-
ence in foodstuffs of PAHs and the human dietary exposure to
these compounds. In a review on food as a source of polycyclic
aromatic carcinogens, Guillen et al. (1997) concluded that the pres-
ence of PAHs in foodstuffs should be reduced to amounts as low as
possible by controlling not only environmental pollution, but also
all procedures that could cause PAH contamination during food
processing, preserving and packaging. Phillips (1999) concluded
that diet was the major source of human exposure to PAHs, with
cereals and vegetables showing the greatest contribution to that
exposure. Ramesh et al. (2004) reviewed the dynamics of PAHs
consumed through the diet and the methods to assess the ex-
tent of risks due to exposure to these pollutants. These authors
remarked that humans were seldom exposed to individual PAHs,
but mostly as complex mixtures, which was of considerable impor-
tance taking into account that PAHs were implicated as causative
agents of breast, lung and colon cancers, among others. Recently,
Zelinkova and Wenzl (2015) extensively reviewed the occurrence
of 16 US EPA PAHs in food, paying special attention to the eval-
uations of the toxicity of PAHs, and the requirements for risk as-
sessment and management stemming from them. The most recent
review on the topic was published by Ma and Harrad (2015), who
summarized reported literature on the presence of PAHs in in-
door air, settled house dust, and food, and highlighted geograph-
ical and temporal trends in indoor PAH contamination. These au-
thors noted that the dietary exposure to PAH ranged from 137 to
55,000 ng/day. No spatiotemporal trends in dietary exposure were
included due to the relatively small number of relevant studies.
The authors noted that while intake via diet and inhalation ex-
ceeded that via dust ingestion, all three pathways contributed and
merited continued assessment (Ma and Harrad, 2015).
In this paper, we present an overview of the available scientic
information on the human exposure to PAHs through the diet, as
well as the dietary health risks for the general population, based
on the criteria recommended by various international organiza-
tions. The inuence of how food is cooked on the concentrations
of PAHs is also reviewed. The scientic literature was reviewed us-
ing the PubMed (http://www.ncbi.nlm.nih.gov/pubmed) and Sco-
pus (http://www.scopus.com/home.url) databases. Some specic
reports (EFSA, US EPA, etc.) were also utilized.
2. Food and PAHs: dietary exposure in a number of countries
Data on the dietary intake of PAHs, as well as benzo[a]pyrene
(BaP), in several countries are summarized in Table 1.
146 J.L. Domingo, M. Nadal / Food and Chemical Toxicology 86 (2015) 144153

Table 1
A summary of publications reporting the dietary intake of benzo[a]pyrene and total PAHs (in g/day)a in a number of countries.

Location Year Daily intake Comments Reference

Benzo[a]pyrene PAHs

Europe Catalonia, Spain 2000 0.128 8.42 Falc et al. (2003)

Catalonia, Spain 2005 0.006 0.268 Only 14 edible marine species Llobet et al. (2006)
Catalonia, Spain 2006 0.089 12.04 Mart-Cid et al. (2008)
Catalonia, Spain 2008 0.076 6.72 Martorell et al. (2010)
Spain 19921996 0.14 8.57 Ibez et al. (2005)
Canary Islands, Spain 2012 1.59 Only eggs Luzardo et al. (2013)
France 20062007 0.013 0.104b Only PAH4d Veyrand et al. (2013)
Uppsala, Sweden 2010 0.049 0.27 Only PAH4d Abramsson-Zetterberg et al. (2014)
Tartu, Estonia 20012005 0.029 0.346 Only meat products Reinik et al. (2007)
Thessaloniki, Greece 19931994 0.005 2.63b Only 5 vegetables species Voutsa and Samara (1998)
United Kingdom n.a. 0.25 3.70 Dennis et al. (1991)
Milan, Italy 19851988 3 Lodovici et al. (1995)
Italy n.a. 0.160.32 n.a. Four mean diet samples Turrio-Baldassarri et al. (1996)
Naples, Italy n.a. 0.153 1.78b Children aged 79 Cirillo et al. (2010)
The Netherlands n.a. 1.122.5 Vaessen et al. (1988)
The Netherlands 19841986 0.120.29 5.2217.06 Low and high estimates De Vos et al. (1990)
Asia Korea n.a. 0.126 n.a. Lee and Shim (2007)
Seoul, Korea 20032004 0.198 Yoon et al. (2007)
Busan, Korea 20052007 1.07 Only 26 marine species Moon et al. (2010)
Korea n.a. 0.002c Only edible oils Kang et al. (2014)
Northern China 19981999 0.106 0.558 Only 9 vegetables species Zhong and Wang (2002)
Taiyuan, China 2008 0.572c Xia et al. (2010)
Xuanwei and Fuyuan, 2009 0.458 14.53 Counties with the highest lung Cai et al. (2012)
China cancer incidence in China
Shanghai, China 20082009 0.848 Yu et al. (2012)
Linzhou, China 2006 0.086b 10.8 Deziel et al. (2013)
Taiyuan, China 2009 0.002 0.061 Nie et al. (2014)
Beijing, China n.a. 1.83b Yu et al. (2015)
Mumbai, India 20062008 0.1240.749 Only sh Dhananjayan and Muralidharan (2012)
America USA 19941996 0.005b n.a. controls vs. cases with Sinha et al. (2005)
colorectal adenoma risk
Brazil 20072008 0.868 Only soybean oils Rojo Camargo et al. (2011)
Africa Nigeria n.a. 3.44e 25.9e Only milk Iwegbue and Bassey (2013)
Nigeria 0.34e 1.62e Only sh Iwegbue et al. (2015)

n.a.: not available.

a
When provided as ng/kg bw/day, dietary intake units were converted to g/day by assuming a mean body weight for the adult population of 70 kg.
b
Median value.
c
g BaP-eq/day.
d
PAH4: benzo(a)pyrene, chrysene, benzo(b)uoranthene, and benz(a)anthracene.
e
Maximum values.

2.1. European countries
The European agro-food sector has major importance/inuence
on the economy of this continent (Yebra-Pimentel et al., 2012).
However, for the countries belonging to the European Union, as
well as for the rest of European countries, information about the
concentrations of PAHs in foodstuffs, as well as on the dietary
intake of these contaminants by the general populations is lim-
ited and notably diversied, depending on each specic country.
Searching in the scientic literature, it can be noted that Spain,
Italy, the Netherlands and the United Kingdom are the countries
with more reported information on the dietary intake of PAHs,
while in other countries such as Azerbaijan, Estonia, France, Greece
and Sweden, the information is limited only to a few studies. On
the other hand, to the best of our knowledge, no estimates on
the dietary intake of PAHs are currently available in the scientic
literature for other European countries. Next, a summary of the
most representative studies is presented according to the respec-
tive countries.
2.1.1. Spain
In 2000, we initiated in our laboratory an extensive study
focused on determining the levels of various environmental con-
taminants, as well as to establish the dietary exposure of the
population living in Catalonia (NE Spain) to those pollutants.
Among the chemical contaminants, 16 PAHs were also included
(Falc et al., 2003). The concentrations of naphthalene, acenaphty-
lene, acenaphtene, uorene, phenanthrene, anthracene, uoran-
thene, pyrene, benz[a]anthracene, chrysene, benzo[b]uoranthene,
benzo[k]uoranthene, benzo[a]pyrene, indeno[1,2,3-c,d]pyrene,
dibenzo[a,h]anthracene and benzo[g,h,i]perylene were determined
in a wide number of foods randomly acquired in local markets,
big supermarkets and grocery stores of seven cities of Catalonia,
from June to August 2000. The food items included in that survey
were the following: meats (fresh beef: steak and hamburger;
pork: loin and sausage; breast chicken, and steak lamb) and meat
products (ham, hot dogs and salami); sh (hake and sardines),
shellsh (mussels) and canned sh (tuna and sardines); eggs;
vegetables and tubers (lettuce, tomatoes, potatoes, green beans,
and cauliower); fruits (apples, oranges and pears); milk (whole
and semi-skimmed) and dairy products (yogurt and cheese),
cereals (bread, pasta, and rice), pulses (lentils and beans), and fats
(margarine) and oils (olive and sunower). Among the analyzed
PAHs, there was a predominance of phenanthrene (16.7 g/kg)
and pyrene (10.7 g/kg). By food group, the highest concentration
of total PAHs was detected in cereals (14.5 g/kg), followed
by meat and meat products (13.4 g/kg), and sh and shell-
sh (7.9 g/kg), while the lowest levels corresponded to fruits
(0.95 g/kg) and vegetables (0.89 g/kg). The dietary intakes of
total and carcinogenic PAHs were calculated for ve population
groups: children, adolescents, male adults, female adults, and
seniors. The mean estimated dietary intakes of the sum of the 16
 J.L. Domingo, M. Nadal / Food and Chemical Toxicology 86 (2015) 144153
PAHs were the following: male adults, 8.4 mg/day; adolescents,
8.2 mg/day; children, 7.4 mg/day; seniors, 6.3 mg/day and female
adults, 6.3 mg/day. In general terms, the highest contributions to
the total dietary intake of PAHs corresponded to cereals, followed
by meat and meat products. Important contributions were also
noted for sh and shellsh, and dairy products. The calculated
daily intake of PAHs would be associated with an increase of 5
cases of cancer for every million inhabitants, taking into account
a population of male adults with a body weight of 70 kg (Falc
et al., 2003).
Considering the important contribution of sh and shellsh to
the dietary intake of most environmental pollutants (including the
PAHs) analyzed in that survey, and taking into account the rela-
tive small number of sh and shellsh species included in that
study (Falc et al., 2003), in MarchApril 2005 samples of 14 ed-
ible marine species were randomly purchased in local sh mar-
kets, large supermarkets, and grocery stores from six large cities
of Catalonia. The analyzed marine species were: sardine, tuna, an-
chovy, mackerel, swordsh, salmon, hake, red mullet, sole, cuttle-
sh, squid, clam, mussel and shrimp. These 14 species are among
those most widely consumed by the Spanish population, includ-
ing that of Catalonia. As in our previous study (Falc et al., 2003),
the concentrations of the 16 PAHs were analyzed in composite
samples of each species. In both studies, and for intake calcula-
tions, when a result was below the limit of detection, that value
was assumed to be one-half of the limit of detection (ND = 1/2
LOD). The highest total PAH concentrations were found in mus-
sel, clam and shrimp (22.4, 21.5 and 15.9 g/kg of fresh weight,
respectively). In contrast, the lowest mean concentrations corre-
sponded to sole (2.5 g/kg of fresh weight), and cuttlesh and
squid (both 3.0 g/kg of fresh weight). Because of their ltering
capacity, bivalves are likely to contain high PAH values, in compar-
ison to other marine organisms (Rey-Salgueiro et al., 2009b). Re-
garding human exposure, the highest PAH intake was observed in
women and girls (5.3 and 5.2 ng/kg/day, respectively), while fe-
male adolescents and female seniors had the lowest PAH intakes
(3.3 ng/kg/day in both groups). Children are a group of special in-
terest. In relation to their body weight, children consume greater
quantities of food than adults, being consequently more relatively
exposed to toxic pollutants. Therefore, we specically estimated
the daily intake of PAHs for children of Catalonia through the con-
sumption of the 14 sh and shellsh species. For both, boys and
girls, daily intake of the 16 PAHs analyzed was 0.12 g. How-
ever, when the calculations were based on body weight, the in-
takes were 5.11 and 5.21 ng/kg/day, for boys and girls, respec-
tively. In fact, children were the age group showing, on average,
the highest intake of the total 16 PAHs (Mart-Cid et al., 2007). On
the other hand, the intake of benzo[a]pyrene and six other PAHs,
which are probably human carcinogens, through consumption of
these marine species, would be associated with 27 cases of can-
cer for every 100 million inhabitants (risk increase of 0.27106 )
over a 70-year life span (Llobet et al., 2006). The main contribu-
tors to the intake of the carcinogenic PAHs were shrimp, hake and
tuna.
In order to assess the temporal trend of the dietary expo-
sure to PAHs by the population living in Catalonia, in March
June 2006, we again collected samples of the foodstuffs most con-
sumed by that population. The 16 PAHs previously determined
(Falc et al., 2003; Llobet et al., 2006) were analyzed in 42 com-
posite samples prepared as in the previous surveys. The dietary
intake of total and carcinogenic PAHs was also estimated for
various age/gender groups of population. The highest individual
PAH concentrations corresponded to phenanthrene (29.66 g/kg),
naphthalene (25.87 g/kg) and uoroanthene (13.66 g/kg),
while the lowest concentrations corresponded to benzo[a]pyrene
(1.28 g/kg), benzo[k]uoranthene (1.31 g/kg) and indeno[1,2,3-
147
c,d]pyrene (1.44 g/kg). Based on the 12 food groups in which
the analyzed food items were divided, the highest contributions
of total PAHs corresponded to the groups of meat and meat
products (25.56 g/kg), oils and fats (23.48 g/kg), and cereals
(20.44 g/kg). For an average male adult (70-kg body weight), the
dietary intake of the sum of PAHs was higher than that found in
our 2000 survey. In that survey (Falc et al., 2003), the mean sum
of the same 16 PAHs for an average male adult was 8.42 g/day,
while the intake of the new survey increased to 12.05 g/day.
However, the carcinogenic risks associated with the dietary intake
of PAHs were similar to those of the 2000 study (Falc et al.,
2003). The mean intake of the seven PAHs considered as proba-
ble human carcinogens by the US EPA (2008), and expressed as in-
take of benzo[a]pyrene equivalents, was 0.248 g/day in 2002 vs.
0.222 g/day in 2006 (Mart-Cid et al., 2008).
Our last total diet study (TDS) was performed in 2008. In
NovemberDecember 2008, we purchased samples of the most
consumed foodstuffs in Catalonia, in 12 cities of that region.
The 16 same PAHs were again determined in composite sam-
ples. Total dietary intake of PAHs for each food group was cal-
culated as in our previous surveys; that is to say, by sum-
ming the results of multiplying the concentration in each spe-
cic food item by the amount (proportionally estimated) consumed
of that food. Finally, total dietary intake was obtained by sum-
ming the respective intakes from each food group. For calculations,
when a concentration was under the respective limit of detec-
tion (LOD), the value was assumed to be equal to one-half of the
LOD (ND = 1/2 LOD). The highest concentrations of PAHs corre-
sponded to phenanthrene (18.18 g/kg), naphthalene (13.31 g/kg)
and pyrene (8.46 g/kg), while the lowest levels corresponded
to dibenzo[a,h]anthracene (0.89 g/kg), indeno[1,2,3-c,d]pyrene
(0.94 g/kg) and benzo[k]uoranthene (1.00 g/kg). With respect
to the contribution of total carcinogenic PAHs, benzo[a]pyrene
contributed 47.77% or 48.22%, depending on the Toxicity Equiva-
lency Factor (TEF) value used. By food groups, the current high-
est levels of total PAHs were detected in meat and meat prod-
ucts (38.99 g/kg), followed by oils and fats (18.75 g/kg) and
dairy products (7.57 g/kg), while the food groups showing the
lowest concentrations of total PAHs were milk (0.47 g/kg), tu-
bers (0.73 g/kg) and fruits (0.81 g/kg). In general terms, these
values were lower than those found in our 2000 study (Falc
et al., 2003). Especially relevant was the important decrease of
PAH levels in cereals (14.45 g/kg vs. 1.27 g/kg). The highest
contribution to the dietary intake of PAHs corresponded to the
group of meat and meat products (4.75 g/day). The estimated
mean dietary intake for a standard male adult (70-kg body weight)
was 6.72 g/day, a lower value than those found in our 2000
(8.42 g/day) (Falc et al., 2003) and 2006 surveys (12.04 g/day)
(Mart-Cid et al., 2008). Regarding to the contribution of car-
cinogenic PAHs, the highest percentages corresponded mainly
to benzo[a]pyrene (48.22%), followed by dibenzo[a,h]anthracene
(34.45%). The food group showing the greatest contribution to
PAHs was meat and meat products (4.75 g/day), followed by oils
and fats (0.51 g/day) (Martorell et al., 2010).
Recently, we also assessed the dietary intake of the same 16
PAHs by the population of Tarragona County (Catalonia, Spain)
using the duplicate diet approach (Martorell et al., 2012). The
results were compared with those from the previous total diet
studies performed in our laboratory (Falc et al., 2003; Mart-
Cid et al., 2008; Martorell et al., 2010). Duplicate diet samples,
prepared as per consumption, were collected during September
2010 in various restaurants offering a variety of daily menus
(breakfast, lunch and dinner). For analysis of PAHs, a total of
90 composite samples were prepared. Due to the specic charac-
teristics of the experimental design of the duplicate diet study,
the average concentrations of each analyzed PAH could not be
148 J.L. Domingo, M. Nadal / Food and Chemical Toxicology 86 (2015) 144153
estimated according to each one of the 12 food groups used
in our previous total diet studies. In the duplicate diet study,
the highest PAH levels corresponded to acenaphthylene, acenaph-
thene and uorene (8.71, 8.24 and 8.04 g/kg, respectively),
while in contrast, benzo[b]uoranthene + benzo[j]uoranthene
and dibenzo[a,h]anthracene showed the lowest levels (0.08 g/kg
in both cases). The highest dietary intakes corresponded to ace-
naphthylene (12.7 g/day), acenaphthene (12.4 g/day) and u-
orene (11.9 g/day), while the lowest intakes corresponded to
dibenz[a,h]anthracene (0.12 g/day), being also comparatively
low those of pyrene, benzo[b]uoranthene, benzo[a]pyrene and
benzo[ghi]perylene (0.13 g/day in all cases). The estimated mean
dietary intake for a standard male adult living in Tarragona County
was 59.2 g/day, an intake 89 times higher than that found in
our previous TDS (6.72 g/day) (Martorell et al., 2010). However,
it is here essential to remark the important methodological differ-
ences existing between both kinds of studies. In general terms, we
concluded that for PAHs, duplicate diet studies might be an alter-
native to total diet studies when there are important economical
limitations to perform a suitable TDS (Martorell et al., 2012), which
seems to offer much more realistic results.
Other investigators have also estimated the dietary intake of
PAHs in Spain. In a study including 40,690 individuals (3564 years
of age) from ve Spanish regions (Catalonia was not included),
Ibez et al. (2005) estimated the dietary intake of PAHs. Cere-
als (40.1%), followed by meat and meat products (20.9%), and by
sh and shellsh (6.1%), were the food groups showing the high-
est contributions to the total dietary intake of PAHs, which was
estimated in 8.57 g/day. The most recent results on the dietary
intake of PAHs by Spanish populations were reported by Luzardo
et al. (2013), who analyzed the levels of 16 PAHs in samples of
eggs, milk and dairy products (cheese, yogurt, butter) randomly
acquired from markets in the Canary Islands. The dietary intake
of PAHs through consumption of these food items was estimated
for children and adults. The mean estimated daily dietary intakes
of the sum of the 16 PAHs were 92.4 and 35.2 ng/kg for children
and adults, respectively. With respect to the carcinogenic potential
of these intakes, the calculated values were associated with addi-
tional 1.6 and 1.9 cancer cases for every million of adults and chil-
dren, respectively, resulting from eating dairy products and eggs.
These results cannot be compared with those of previous studies
in Spain, as the number of foodstuffs included in this last study
was much more limited.
Other authors have reported the concentrations of PAHs in var-
ious food samples purchased from different areas (Barranco et al.,
2004; Fontcuberta et al., 2006; Guilln et al., 2011). However, the
dietary intake and/or the health risks were not estimated, or re-
ported.
2.1.2. Italy
The rst data on estimated dietary intake of PAHs by the Italian
population were reported by Lodovici et al. (1995), who found that
cereals, milk products, meats, and vegetables and fruits were the
food groups meaning the highest contribution to the dietary PAH
intake. The total dietary PAH intake was 3 g/day, while the esti-
mated intake of carcinogenic PAHs was 1.4 g/day. The high con-
sumption of contaminated cereal products was the main respon-
sible of the PAH intakes, being the highest levels of PAHs found
in pizza baked in wood-burning ovens, as well as in barbecued
beef and pork. In turn, Turrio-Baldassarri et al. (1996) analyzed
8 PAHs in four mean Italian diet samples. Benzo[a]pyrene intakes
were 0.17, 0.32, 0.19, 0.16 g/day, in each of those diets, respec-
tively. Cirillo et al. (2010) investigated the dietary exposure to 16
PAHs in primary school children (79 years old) of Naples using a
one-week duplicate diet sample analyses. The benzo[a]pyrene me-
dian concentrations in foods varied from 0.06 to 0.33 g/kg. The
daily median intakes of benzo[a]pyrene, benzo[a]pyrene + chry-
sene (PAH2), PAH2 + benz[a]anthracene + benzo[b]uoranthene
(PAH4), PAH4 + benzo[k]uoranthene + benzo[ghi]perylene +
dibenzo[a,h]anthracene + indeno[1,2,3-c,d]pyrene (PAH8) were
153, 318, 990 and 1776 ng/day, being their median exposures 5,
10, 28 and 54 ng/kg/day, respectively.
Other authors also determined the levels of PAHs in various
food items of the Italian market such as olive oils (Menichini et al.,
1991), marine organisms (Amodio-Cocchieri et al., 2003; Perug-
ini et al., 2007), smoked seafood (Storelli et al., 2003), frying oils
and snacks (Purcaro et al., 2006), and smoked buffalo mozzarella
cheese (Fasano et al., 2015). However, these investigations only re-
ported PAH levels in specic food items.
2.1.3. The Netherlands
Vaessen et al. (1988) estimated the intake of PAHs in the
Netherlands from PAH concentrations determined in 50 dupli-
cate portions of 24-hour diets. The highest levels were found in
mussels and kale, being the ranges of total PAHs (15 individ-
ual PAHs were analyzed) in mussels 124384 g/kg and in kale
46219 g/kg. Total dietary PAH intake ranged between 1.1 and
22.5 g/day. Results indicated that 30% of the oral intakes were
carcinogens. In a market basket study carried out by De Vos et al.
(1990), 17 PAHs were analyzed in 221 food items. The most fre-
quently occurring PAHs were benzo[b]uoranthene, uoranthene
and benzo[k]uoranthene, which were detected in 59, 48 and
46% of the samples, respectively. For a population of 18-year old
males, the daily intake of the analyzed PAHs was calculated, be-
ing the mean intake of the total PAHs between 5 and 17 g/day.
In turn, the intake of the carcinogenic PAH fraction was approxi-
mately one-half of these amounts. The highest contribution to this
intake corresponded to sugar and sweets, cereals, oils, fats and
nuts.
On the other hand, the urinary 1-hydroxypyrene level as an in-
dicator of exposure to PAHs, was determined in Dutch adult vol-
unteers (van Rooij et al., 1994) and in randomly selected Dutch
children aged 16 years (van Wijnen et al., 1996) showing in both
surveys that the diet was the main route of exposure to PAHs.
2.1.4. United Kingdom
Dennis and co-workers (1991) performed a total-diet analysis
in order to estimate the dietary intake of 12 PAHs, as well as to
establish the types of foodstuffs, which probably were the high-
est dietary sources of PAHs. It was found that cereals and oils/fats
were the main contributors of PAHs in the total diets, with about
one-third each. In contrast, meat, sh, milk and beverages showed
the minor contributions. The dietary intake of PAHs ranged be-
tween 0 and 1.09 g/day for indeno[1,2,3-c,d]pyrene and pyrene,
respectively. The total dietary intake of PAHs was estimated in
3.70 g/day, assuming a total daily consumption of 1.46 kg of food
and beverages. When the factors affecting (PAH) concentrations in
cereals, oils/fats, and other foodstuffs were investigated, the levels
of PAHs were found to be low in retail sh and animal-derived oils
and fats such as butter (Dennis et al., 1991). In an extensive review
by Phillips (1999), it was concluded that the diet contributed sig-
nicantly to the non-occupational exposure to PAHs, being more
than 70% of exposure for non-smokers attributable to the diet.
Phillips (1999) also carefully reviewed the differences in the di-
etary exposure to PAHs between uncooked and cooked food, an
issue which will be specically discussed later in the current ar-
ticle.
2.1.5. Other European countries; Azerbaijan, Estonia, France, Greece
and Sweden
Although Nwaneshiudu et al. (2007) calculated the risks for
adults and children of Azerbaijan derived from the daily inges-
 J.L. Domingo, M. Nadal / Food and Chemical Toxicology 86 (2015) 144153
tion of 15 PAHs, the mean daily intake by the Azeri population
was not estimated/reported. The concentration data from different
sources representing international studies carried out in previous
years were used to determine the food items that contributed to
the highest dietary exposure to PAHs for the Azeri population. Due
to the lack of data from middle-Eastern countries, only data from
European countries were used in that study (Nwaneshiudu et al.,
2007). An estimate of the risks associated with food intake of PAHS
was determined within a range of uncertainty. Children risks were
between 4 and 7 times higher than those corresponding to adult
risks. Eggs, bread and bakery products, and milk and dairy prod-
ucts, were the main contributors to the carcinogenic risks.
As a part of a food safety monitoring program carried out be-
tween 2001 and 2005 in Estonia, Reinik et al. (2007) determined
the levels of 12 PAHs in 322 commercial, cured meat products,
and 14 home-grilled meat samples. The highest PAH concentra-
tions were detected in home-grilled pork samples. The average in-
take of BaP and the sum of 12 PAHs from meat products was es-
timated for children (aged 116 years), on the basis of an indi-
vidual food consumption questionnaire, as well as for the general
population, based on national food consumption data. The high-
est total PAH concentrations detected were 16 g/kg in smoked
meat and ham, 19 g/kg in smoked sausage, and 6.5 g/kg in
smoked chicken samples. The mean BaP intake by Estonian chil-
dren was found to be 14 ng/day, being the intake of all analyzed
PAHs from meat products, 192 ng/day. For the general population,
these intakes were 29 and 346 ng/day, for BaP and total PAHs,
respectively.
In France, in the frame of the second French TDS, Veyrand
et al. (2013) analyzed the concentrations of 16 PAHs in 725
foodstuffs widely consumed by the French population. By food
groups, the highest concentrations of total PAH were found in mol-
lusks and crustaceans (4.3 g/kg), oils (1.9 g/kg), and margarine
(1.3 g/kg). Mean exposures to the sum of PAH4 (benzo[a]pyrene,
benz[a]anthracene, chrysene and benzo[b]uoranthene) were esti-
mated to be 1.48 and 2.26 ng/kg/day for adults and children, re-
spectively. The main contributors to PAH exposure for adults were
fats, bread and dried bread products, followed by crustaceans and
mollusks, while for children the main contributors were cereal
products and oils. In a previous French estimation of the dietary
exposure to 6 PAHs, the mean exposure was 4.9 ng/kg/day, a value
approximately 3-times higher than the PAH4 exposure estimated
in the study of Veyrand et al. (2013).
In Greece, Voutsa and Samara (1998) estimated the intake of 16
PAHs via consumption of some vegetables (cabbage, carrot, leek,
lettuce and endive) grown in an industrial area. The intake ranged
from 1.6 to 4.5 g/person/day, being the highest with leafy vegeta-
bles. As only 5 vegetables were included in that study, the compar-
ison of the daily intake with total diet studies performed in other
countries is obviously unviable. However, in a study carried out in
our laboratory (Falc et al., 2003) the contribution of vegetables
and tubers to the total intake of PAHs was 0.467 g/person/day,
a notable lower value. This relevant difference would be explained
taking into account that in the Greek study vegetables were ob-
tained from a polluted industrial area.
Recently, Abramsson-Zetterberg et al. (2014) reported the re-
sults of a market basket study made at the National Food Agency
(NFA) of Sweden, where the concentrations of BaP and PAH4 (BaP,
chrysene, benzo[b]uoranthene, and benz[a]anthracene) were an-
alyzed in the most common consumed foodstuffs of that country.
The mean intakes of BaP and PAH4 by the Swedish populations
were estimated to be 49 and 270 ng/person/day, respectively, with
sugar and sweets, cereals, meat and dairy being the products with
the highest contribution to the total PAH intake. A market bas-
ket study made at the NFA in the same way in 1999, had shown
that the concentration of PAHs in food decreased during the last
149
years. It was concluded that the lower PAH levels might be due
to improved production processes and also because of lower air
pollution.
2.2. Asia
2.2.1. China
Zhong and Wang (2002) analyzed the levels of anthracene, u-
oranthene, benz(a)anthracene and benzo[a]pyrene in samples of 9
vegetables collected from northern Chinese market. The mean con-
centrations were 6.46, 4.05, 3.33, 4.51 g/kg, respectively, with
leafy and stem vegetables showing higher PAH contents than
root and fruit vegetables. Among the analyzed vegetables, scal-
lion (1.93 g/person/day) was the most important source of expo-
sure to PAHs, followed by potato (1.06 g/person/day) and cabbage
(1.02 g/persona/day). In contrast, eggplant (0.43 g/person/day)
showed the lowest contribution to PAHs. However, due to the ge-
ographic and demographic characteristics of China, the authors
specically remarked that the study was not designed to be sta-
tistically representative for China, as a whole. In turn, Tao et al.
(2004) analyzed the concentrations of 16 PAHs in samples of eight
vegetable species collected at two polluted sites (named A and
B) in Tianjin (northern China). The highest levels of PAHs were
found in cauliower (0.85 g/g and 1.69 g/g for sites A and
B, respectively), followed by celery (0.64 g/g and 1.41 g/g). In
contrast, turnip showed the lowest concentrations of PAHs (0.34
and 0.78 g/g for sites A and B, respectively). The authors re-
ported that, on average, the PAH levels in the aerial part of veg-
etables were 6.5 times higher than those found in roots. Notwith-
standing, no intake estimations were done in that study. Xia
et al. (2010) analyzed the concentrations of 16 PAHs in 25 food-
stuffs belonging to seven categories of food, which were pur-
chased in supermarkets, wholesale markets and community farm-
ers markets in Taiyuan, the capital of Shanxi Province, and one
of the great industrial cities of northeastern China. The high-
est levels of total PAHs were found in pork (195.30 g/kg), fol-
lowed by beef and mutton (189.00 g/kg), sh (160.30 g/kg)
and chicken (87.49 g/kg), while the lowest levels were found in
milk (8.73 g/kg) and vegetables (20.60 g/kg). The median values
of B[a]P equivalent (B[a]P(eq)) exposure doses for children, ado-
lescents, adults and seniors were estimated to be 392.42, 511.01,
571.56 and 532.56 ng/day for males, and 355.16, 440.51, 487.64 and
444.85 ng/day for females, respectively.
Cai et al. (2012) assessed the dietary exposure to 16 PAHs in
Xuanwei and Fuyuan, two counties in the southwest of China,
which has the highest lung cancer incidence in that country.
The exposure to BaP, total PAHs, and toxic equivalents, based on
benzo[a]pyrene, were estimated to be 458 ng/day, 14,532 ng/day,
and 896 ng/day, respectively. These intakes are notably lower than
those found in other Chinese cities. Dietary exposure was not, in
general terms, the main exposure route of PAHs, which means
that there was not a direct relationship between dietary expo-
sure and the high lung cancer incidence in the analyzed areas.
In another survey also related with the unusual high incidence of
cancer in certain areas of China, Deziel et al. (2013) determined
the levels of 14 PAHs in air and food of 20 non-smokers over
multiple days, and compared the concentrations with a urinary
PAH biomarker, 1-hydroxypyrene glucuronide (1-OHPG). The me-
dian daily food BaP concentration and intake were 0.08 g/kg and
86 ng/day (IQR = 41142 ng/day), respectively. The intraclass cor-
relation coecients (ICCs) for daily food concentrations of naph-
thalene, pyrene, and benzo[a]pyrene were 0.36, 0.03, and 0.15, re-
spectively. The PAH concentrations found in air, food and urine
demonstrates that the population living in the area (Linzhou) as-
sessed, is highly exposed to PAHs. Therefore, the authors strongly
recommended further evaluation of the potential etiologic role of
150 J.L. Domingo, M. Nadal / Food and Chemical Toxicology 86 (2015) 144153
PAH exposure in the elevated rates of esophageal cancer in that
area of China, including that of dietary exposure.
Yu et al. (2012) determined the levels of 15 PAHs in 175
samples of 18 types of food purchased from markets in Shang-
hai. Among the compounds measured, phenanthrene was the pre-
dominant PAH. The mean levels of PAHs varied between 2.4 and
47.1 g/kg, while the intake of PAHs through foodstuffs, by an av-
erage Shanghai resident, was 848 ng/day. Interestingly, the intake
decreased to 297 ng/day when the bioaccessibility of PAHs was
considered, suggesting that most intakes might have been over-
estimated. On the other hand, Nie et al. (2014) determined the
levels of 16 PAHs in 24 duplicate-diet samples in Taiyuan City
(Shanxi Province). Vegetables, wheat our, and fruits were the
main sources of dietary PAHs, with the sum contributing with
75.95% of PAHs. Among the analyzed PAHs, the highest contri-
bution corresponded to benzo[a]pyrene, followed by indeno[1,2,3-
c,d]pyrene. The total PAH intake was estimated in 6075 ng/day.
Given as B[a]P(eq), the intake was 2.54 or 0.26 ng/day, depending
on whether it corresponded to cooked food, or raw food, respec-
tively. According to Nie et al. (2014), the cooking process might
introduce more B[a]P(eq) into food, and the relative contribution
of 16 PAHs in the diet would change during cooking. The inuence
of cooking on the dietary intake of PAHs is discussed later in the
current paper. Recently, Yu et al. (2015) performed a study whose
main objectives were: 1) to determine the exposure levels of the
Beijing population to 15 PAHs through the diet and inhalation, 2)
to establish the main contributors to dietary and inhaled exposure
to PAHs in that population, and 3) to assess the cancer risks for
the Beijing population caused by PAH exposure. The estimated me-
dian dietary exposure levels (ng/person/day) of the sum of the 15
PAHs, for eight subgroups of the Beijing population, were between
1.37 104 for female girls and 1.92 104 for male adolescents.
When the dietary exposure was estimated with body weight ad-
justment (ng/kg/day) the median intakes ranged between 241 for
female seniors and 574 for male boys. Meat and cereals were the
main sources of dietary exposure to PAHs.
2.2.2. Korea
Lee and Shim (2007) analyzed BaP concentrations in vari-
ous foods to estimate the dietary intake of this PAH in or-
der to assess the related-cancer risks in Koreans. In terms of
chronic daily intake of BaP, fried chicken was shown to be
the highest (70.09 ng/person), while perilla oil was the lowest
(0.05 ng/person). The total intake of BaP due to the consump-
tion of the food items investigated in that study was estimated
to be 124.55 ng/person, being the dietary BaP-related cancer risk
1.52 105 . Yoon et al. (2007) analyzed the levels of 14 PAHs
in 27 food items widely consumed by the Korean population.
The total PAH (TEQ-BaP) levels in foods ranged between 0.040
(fruits) and 1.234 g/TEQ-BaP/kg (roast laver, which is a kind of
seaweed). The lifetime average daily intake was estimated to be
3.22 103 g TEQ/kg, with notable differences depending on
the groups of age of the consumers. The foodstuffs showing the
highest contribution to the dietary intake were cooked rice, milk,
Korean cabbage kimchi and eggs. The dietary excess cancer risk
estimated using the cancer potency of BaP (7.3 kgday/mg) was
2.3 105 , which is equivalent to a probability of tumor eruption
in the upper gastrointestinal tract of two per hundred thousand
persons.
On the other hand, Moon et al. (2010) measured the concen-
trations of 16 PAHs in 26 types of marine species commonly con-
sumed by the general Korean population. The concentrations of the
sum of PAHs and the sum of carcinogenic PAHs ranged from 12.3
to 243 g/kg, and from 0.21 to 18.4 g/kg, respectively. The high-
est concentration of the sum of PAHs in marine species was found
in ounder, while bivalves, such as clam, oyster and ark shell,
also showed relatively high concentrations. In general terms, lev-
els of the sum of PAHs were higher in bivalves (6.38 4.35 g/kg
dry weight) than in sh species (0.99 1.41 g/kg dry weight).
The average intake of PAHs through seafood consumption in Ko-
rea was estimated to be 15.3 ng/kg body weight/day (16.7 and
13.8 ng/kg body weight/day, for Korean mean and women, respec-
tively). Among the species analyzed, squid contributed to the high-
est intake (2.31 ng/kg body weight/day), accounting for 15.1% of
total PAH intake, followed by mackerel (12.9%) and yellow croaker
(10.7%). In contrast, the lowest contribution corresponded to her-
ring (0.2%), and mussel and lesh (both 0.4%). On the other hand,
Kang et al. (2014) recently determined the levels of 8 PAHs in edi-
ble oils commonly consumed by the population of Korea. Exposure
to PAHs from the consumption of edible oils was only 0.025 ng/kg
body weight/day, an intake considerably lower than those from
marine species reported previously by Moon et al. (2010). The es-
timated excess cancer risk values from seafood consumption for
the general population were 2.85 106 for the general popu-
lation, and 2.93 106 and 2.68 106 , for men and women,
respectively. In another survey, in which the concentrations of 16
PAHs were determined in 280 samples of marine products of the
Korean market, Hwang et al. (2012) reported sums of total PAH
concentrations in the ranges of 0.20.5, 1.21.6 and 0.81.9 g/kg,
for the groups of sh, shellsh, and cephalopods/crustacean,
respectively.
2.2.3. India
A number of authors have reported the occurrence of PAHs in
Indian food. However, most of these have focused only on spe-
cic food items, such as vegetables (Tuteja et al., 2011) and sh
(Chatterjee et al., 2015). Pandey et al. (2004) analyzed the levels of
PAHs in 296 samples of edible oil purchased from local retail mar-
kets of Lucknow, India. Virgin olive oil showed the highest levels
of PAHs (624 g/kg), while the lowest PAH content was found in
rened vegetable oils (40.2 g/kg). The maximum dietary intake
of total PAHs through the consumption of oils corresponded to im-
ported olive oil, with a mean intake of 20.8 g/day, being 42% the
contribution of heavy hydrocarbons. In turn, Dhananjayan and Mu-
ralidharan (2012) reported the concentrations of PAHs in 5 species
of sh samples collected along the harbour line of Mumbai, India,
between 2006 and 2008. The concentration of total PAHs ranged
from 17.43 to 70.44 g/kg, and the estimated intakes of PAHs by
sh consumption for the general population were ranged between
1.77 and 10.70 ng/kg bw/day.
2.3. America
2.3.1. USA
Howard and Fazio (1980) reviewed available data on concen-
trations of PAHs found in surveys carried out in USA in the 1970s.
They noted that the levels of PAHs were essentially unchanged dur-
ing the last 10 years, but the dietary intake of PAHs for the USA
population was not estimated. One of the most complete US stud-
ies on human dietary exposure to PAHs, and more specically to
BaP, was performed by Kazerouni et al. (2001), who analyzed 200
food items for BaP and estimated its intake by the population of
Washington, D.C. It was found that the food items with the high-
est concentration of BaP were very well done grilled/barbecued
steak, well done grilled/barbecued chicken with skin, very well
done grilled/barbecued hamburger, collard greens and kale, pump-
kin pie, pretzels, bran and granola cereal, cooked cereal, margarine
and French fries. The authors reported that the bread/cereal/grain
group, followed by the grilled/barbecued meat group, contributed
the most to the percent of total daily BaP intake in the control
subjects. It was found that cereals contributed 29% to the mean
 J.L. Domingo, M. Nadal / Food and Chemical Toxicology 86 (2015) 144153
daily intake of this pollutant, while grilled/barbecued meat con-
tributed 21%. The benzo[a]pyrene intake levels for approximately
31% of the subjects ranged from 0.040 to 0.060 mg/day, while the
intake levels for about 27% of the subjects ranged from 0.060 to
0.180 mg/day. In another survey, Sinha et al. (2005) performed a
clinic-based case-control study aimed at addressing if dietary in-
take of PAHs was associated with colorectal adenoma risk. BaP in-
take, derived from meat and from all other consumed foods, was
estimated to test its relationship with risk of colorectal adenomas.
The median BaP intake in controls was 5 ng/day estimated from
meat, and 73 ng/day from the rest of foods. Increased risk of col-
orectal adenomas was more strongly associated with BaP intake
estimated from all foods other than meat. It was concluded that
dietary BaP played a role in colorectal adenoma etiology.
2.3.2. Brazil
Rojo Camargo et al. (2011) analyzed 13 PAHs in 42 samples of
different brands of soybean oils available on the Brazilian mar-
ket. The presence of PAHs was detected in all the samples, with
mean summed PAH levels ranging from 10.4 to 112.0 g/kg. Conse-
quently, the mean and maximum dietary exposures for total PAHs
were estimated as 12.4 and 19.1 ng/kg/day, respectively. Similarly
to other countries, information on the dietary intake of PAHs is
very scarce (if any), being some studies limited to quantify the lev-
els of these compounds in some specic food items, such as raw
cane sugar (rapadura) or soybean oils (Rojo Camargo et al., 2012;
Silva et al., 2011).
2.4. Africa
There is currently no information regarding the dietary intake
of PAHs by the population of any African country, according to
the bibliographic search performed. The only limited studies are
aimed at evaluating the occurrence of PAHs in some specic foods.
Akpambang et al. (2009) determined the PAH contents of different
smoked or grilled meat and sh products commonly consumed in
Nigeria. Samples that were smoked or grilled using traditional sys-
tems, which use a wood re, were heavily contaminated with BaP
(range: 2.431.2 g/kg). Iwegbue and Bassey (2013) analyzed the
concentrations and proles of PAHs in twenty popular commer-
cial brands of milk from the Nigerian market, being the dietary
intake of PAH8 estimated in a maximum level of 369.6 ng/kg/day.
The same authors recently reported PAH levels in 10 popular sh
species in Nigeria (Iwegbue et al., 2015). Benzo[a]pyrene occurred
in 23% of these sh samples at concentrations above the European
Union permissible limit of 2.0 g/kg.
On the other hand, Essumang et al. (2013) analyzed the PAH
levels in 108 samples of four different smoke-cured sh (mackerel,
sardine, tuna and Cigar minnows), and reported mean BaP levels
for most sh cured with smoke from acacia and mangrove well
above European standards.
3. Inuence of cooking procedures on the concentrations of
PAHs in food
When the scientic literature was carefully analyzed, we noted
that in most reported studies on the dietary intake of chemi-
cal pollutants, food analyses were almost exclusively performed
in uncooked/raw products. Although it is well known that the
physicochemical and nutritional characteristics of foodstuffs can be
widely modied by cooking processes, studies focused on the ef-
fects of cooking on the potential changes (increases or decreases)
of chemical contaminants in food are rather limited (Kazerouni
et al., 2001; Reinik et al., 2007; Perell et al., 2008, 2009; Ericson-
Jogsten et al., 2009; Domingo, 2011). PAHs are not an exception,
being very scarce the available information on the inuence of
151
cooking processes on the levels of PAHs in foodstuffs. Kazerouni
et al. (2001) analyzed cooked samples of meat and other non-meat
items by different techniques in controlled conditions. The high-
est levels of BaP were found in grilled/barbecued very well done
steaks and hamburgers, as well as in grilled/barbecued well done
chicken with skin. BaP concentrations were lower in meats that
were grilled/barbecued to medium done and in all broiled or pan-
fried meat samples (regardless of doneness level). Although the
BaP levels in non-meat items were generally low, certain cereals
and greens (e.g. kale, collard greens) had levels of up to 0.5 g/kg.
The contributions to the mean daily intake of BaP were 29%
and 21% for the bread/cereal/grain, and grilled/barbecued meat,
respectively. Storelli et al. (2003) reported higher levels of sev-
eral lipophilic pollutants, including PAHs, in smoked seafood. To-
tal PAH concentrations ranged from 46.5 g/kg for smoked sword-
sh to 124.0 g/kg for smoked herring. Among the carcinogenic
PAHs, benzo[a]pyrene ranged from undetectable levels for sev-
eral smoked sh to 0.7 g/kg for Scottish salmon. In turn, Reinik
et al. (2007) analyzed the concentrations of BaP and 11 other
PAHs in samples of meat products and meats prepared accord-
ing to traditional Estonian practices, among which, smoking and
grilling are prevalent meat-cooking methods in Estonia. The high-
est total levels of PAHs were 16 g/kg in smoked meat and ham,
19 g/kg in smoked sausage, and 6.5 g/kg in smoked chicken
samples.
In our laboratory, we assessed the inuence of cooking on
the concentrations of 16 individual PAHs in a total of 68 com-
posite samples of various foodstuffs (meats, sh, vegetables, rice
and olive oil). Samples were subjected to four cooking proce-
dures: fried, grilled, roasted and boiled. The highest concentrations
of the sum of the 16 PAHs, as well as that of the carcinogenic
PAHs were found, in general terms, after frying, being the con-
centrations especially notable in sh (excepting hake, for which
the highest total PAH concentrations corresponded to roasted sam-
ples) (Perell et al., 2009). In relation to the 7 carcinogenic PAHs,
only dibenzo[a,h]anthracene could not be detected in any sample.
The highest sum of total carcinogenic PAHs was found in olive oil
samples, followed by fried sardine and fried tuna. The results of
that study corroborated those of other investigations on the inu-
ence of cooking on the concentrations of some chemical contam-
inants in foodstuffs, not showing a direct and/or signicant cor-
relation between the type of cooking and the observed changes (if
any), which mainly would depend on the cooking conditions: time,
temperature and medium of cooking (Ericson-Jogsten et al., 2009;
Perell et al., 2009; Domingo, 2011).
4. Summary and conclusions
After having carried out an extensive review of the reported
scientic literature on the dietary intake of PAHs, we highlight
the notable absence of data from big countries such as Australia,
Canada, Germany, or Japan (for example), among many others. It
seems rather unusual based on the important scientic and social
interest that the knowledge of the health risks of human exposure
to environmental pollutants raises in those countries, where it is
an issue of great concern.
The comparison of the dietary intakes of PAHs for the above re-
viewed studies shows very notable differences. These differences
may be explained by a number of factors. Probably, the most im-
portant is the different methodologies used in the different sur-
veys. It concerns not only to the foodstuffs included in the respec-
tive studies, but also, and this is very relevant, to the different (also
in number) PAHs analyzed in those studies. Thus, some studies
were focused on BaP only, while others determined various PAHs
(including BaP), while the concentrations of the 16 US EPA PAHs
were measured in a number of studies. In addition, estimations of
152 J.L. Domingo, M. Nadal / Food and Chemical Toxicology 86 (2015) 144153
the intakes have been done for different groups of age and gender,
which adds diculties for the comparison among studies. Even for
those surveys that were performed through a TDS, the considerable
differences in the dietary habits of the populations of the different
countries make complex comparing the dietary intakes of PAHs, as
well as the derived health risks. Finally, some studies assessed the
risks of the carcinogenic PAHs only, while others covered also the
non-carcinogenic PAHs.
With respect to temporal trends in the human exposure to
PAHs through the diet, the information is very limited. In fact, it
is based only on the studies performed in our laboratory (Catalo-
nia, Spain) throughout recent years (Falc et al., 2003; Mart-Cid
et al., 2008; Martorell et al., 2010). In the last survey of that se-
ries, the estimated mean dietary intake of 16 PAHs for a standard
male adult (70-kg body weight) was 6.72 g/day (Martorell et al.,
2010), a lower value than those found in our 2000 (8.42 g/day)
(Falc et al., 2003) and 2006 surveys (12.04 g/day) (Mart-Cid
et al., 2008). These intakes are very different than that also found
in our laboratory, 59.2 g/day, when it was estimated through a
duplicate diet study (Martorell et al., 2012). This may be a clear
example of the notable differences in the results found among the
above reviewed studies, which depend on the methodology used.
In relation to the inuence of the cooking procedures (e.g., fry-
ing, grilling, boiling, or roasting) on the levels of PAHs in foodstuffs
and the dietary intake, it has been shown that certain cooking pro-
cesses could reduce or increase the levels of chemical contami-
nants in food, in general, and those of PAHs in particular (Domingo,
2011). However, it seems that the inuence of cooking on the lev-
els of the contaminants (including PAHs) depends, not only on the
particular cooking process, but even more on the characteristics
of each specic food item. In general terms, cooking procedures
that release or remove fat from the product should tend to re-
duce the total concentrations of the organic contaminants in the
cooked food. As human exposure to PAHs via the diet is, with
inhalation, the main pathway of exposure to these compounds
(Ma and Harrad, 2015), considering the tremendous inuence on
the environmental levels of PAHs on their concentrations in food-
stuffs, a signicant reduction of the environmental PAHs should
reduce simultaneously the inhalation and dietary intake of these
pollutants.
Conict of interest
The authors declare that there are no conicts of interest.
Transparency document
Transparency document related to this article can be found on-
line at http://dx.doi.org/10.1016/j.fct.2015.10.002.
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