title: Biomarkers of exposure to combustion by-products in a human population in Shanxi, China.
abstract: Emissions of complex mixtures of polycyclic aromatic hydrocarbons (PAHs) and other compounds into the environment represent a potential threat to the health of humans. Information regarding the dose and duration of exposure is essential to determine the degree of risk and to identify sensitive receptors within a population. Although measurements of chemical concentrations in air may be used to estimate exposures, internal biomarkers provide more accurate information regarding the dose of exposure and retention of toxic chemicals. This study was conducted in a population in rural China exposed to PAHs from a variety of sources. The study population was located in an area known to have an elevated incidence of birth defects. Parents of children born with a neural tube defect (NTD) were recruited as case participants and parents of children born with no visible birth defect were recruited as controls. The study was designed to test the hypothesis that parents of children born with a NTD would exhibit a biomarker of exposure at higher levels than the parents of a child with no visible birth defect. A total of 35 mothers and 32 fathers were recruited as case participants, and 18 mothers and 19 fathers were recruited as control participants. Venous blood was collected from the study participants by hospital staff as soon as possible following the birth of the child. PAHs were isolated from the whole blood by solvent extraction and DNA was isolated from a separate aliquot of blood for (32)P-postlabeling to measure bulky adducts. Single Nucleotide Polymorphisms (SNPs) in phase II enzymes were also monitored in an attempt to identify sensitive receptors. Both total and carcinogenic PAH (cPAH) concentrations were elevated in the parents of case children. Both values were elevated significantly in mothers, whereas only cPAH concentrations were elevated significantly in fathers. Levels of DNA adducts were highly variable and displayed a reverse pattern to that of PAH levels in blood. None of the polymorphisms evaluated were correlated with PAH levels or DNA adducts. For mothers, whose total PAH concentration was above the median concentration, the age-adjusted odds ratio (OR) for having a child with a NTD was 8.7. Although this suggests that PAHs may be a contributing factor to the risk of NTDs, the lack of a correlation with DNA adducts would suggest a possible non-genotoxic mechanism. Alternatively, the PAHs may be a surrogate for a different exposure that is more directly related to the birth defects. The results have shown that blood levels of PAHs may be used to identify populations exposed to elevated concentrations of combustion by-products.
authors.affiliation: Department of Environmental and Occupational Health, Texas A&M Health Science Center, School of Rural Public Health, College Station, Texas 77843-1266, USA.
authors.forename: Ziad
authors.initials: Z
authors.lastname: Naufal
authors.forename: Li
authors.initials: L
authors.lastname: Zhiwen
authors.forename: Li
authors.initials: L
authors.lastname: Zhu
authors.forename: Guo-Dong
authors.initials: GD
authors.lastname: Zhou
authors.forename: Thomas
authors.initials: T
authors.lastname: McDonald
authors.forename: Ling Yu
authors.initials: LY
authors.lastname: He
authors.forename: Laura
authors.initials: L
authors.lastname: Mitchell
authors.forename: Aiguo
authors.initials: A
authors.lastname: Ren
authors.forename: Huiping
authors.initials: H
authors.lastname: Zhu
authors.forename: Richard
authors.initials: R
authors.lastname: Finnell
authors.forename: Kirby C
authors.initials: KC
authors.lastname: Donnelly
mesh_terms: D000328:Adult; D000397:Air Pollution / Q000009:adverse effects*; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D002681:China; D018736:DNA Adducts / Q000097:blood*; D005260:Female; D005982:Glutathione Transferase / Q000235:genetics; D006801:Humans; D008297:Male; D018811:Maternal Exposure / Q000009:adverse effects*; D009436:Neural Tube Defects / Q000097:blood / Q000209:etiology*; D018812:Paternal Exposure / Q000009:adverse effects*; D011084:Polycyclic Aromatic Hydrocarbons / Q000009:adverse effects / Q000097:blood*; D020641:Polymorphism, Single Nucleotide; D012307:Risk Factors; D012424:Rural Population
chemical_list: D015415:Biomarkers; D018736:DNA Adducts; D005982:Glutathione Transferase; D011084:Polycyclic Aromatic Hydrocarbons; C413545:glutathione S-transferase T1