Exposure Profile (exposure + profile)

Distribution by Scientific Domains


Selected Abstracts


Association between asbestos exposure, cigarette smoking, myeloperoxidase (MPO) genotypes, and lung cancer risk

AMERICAN JOURNAL OF INDUSTRIAL MEDICINE, Issue 1 2002
Matthew B. Schabath MS
Abstract Background As observed in tobacco-associated carcinogenesis, genetic factors such as the polymorphic metabolic/oxidative enzyme myeloperoxidase (MPO) could modulate individual susceptibility to asbestos-associated carcinogenesis. Methods RFLP-PCR analysis identified the MPO genotypes in 375 Caucasian lung cancer cases and 378 matched controls. An epidemiological interview elicited detailed information regarding smoking history and occupational history and exposures. Results Asbestos exposure was associated with a significantly elevated risk estimate (OR,=,1.45; 95% CI 1.04,2.02). On stratified analysis, we found the MPO genotypes modified the effect of asbestos exposure on lung cancer risk. Specifically, G/G carriers who were exposed to asbestos had an odds ratio (OR) of 1.72 (95% CI; 1.09,2.66), while A-allele carriers (G/A,+,A/A) exposed to asbestos exhibited a reduced OR of 0.89 (95% CI; 0.56,1.44). The OR was further reduced to 0.73 (0.49,1.06) for A-allele carriers not exposed to asbestos. A similar trend was observed for the joint effects between the MPO genotypes and pack-years smoking. Next, all three risk factors (MPO genotypes, asbestos exposure, and smoking) were analyzed simultaneously for joint effects. Heavy smokers with the G/G genotype and a history of asbestos exposure demonstrated a statistically significant elevated risk estimate (OR,=,2.19; 95% CI 1.16,4.11), while the A-allele carriers with the same exposure profile were at a lower risk for lung cancer (OR,=,1.18; 95% CI 0.58,2.38). The A-allele genotypes demonstrated similar protective effects for the other three exposure profiles. Conclusions For a similar level of exposure to established carcinogens, individuals with the MPO A-allele genotypes appear to have a reduced risk of lung cancer. Am. J. Ind. Med. 42:29,37, 2002. © 2002 Wiley-Liss, Inc. [source]


The association between socioeconomic status and exposure to mobile telecommunication networks in children and adolescents

BIOELECTROMAGNETICS, Issue 1 2010
Silke Thomas
Abstract A potential association between socioeconomic status (SES) and self-reported use of mobile phones has been investigated in a few studies. If measured exposure to mobile phone networks differs by SES in children, it has not yet been studied. Interview data of 1,481 children and 1,505 adolescents on participants' mobile phone use, socio-demographic characteristics and potential confounders were taken from the German MobilEe-study. Sociodemographic data was used to stratify participants into three "status groups" (low, middle, high). Using a personal dosimeter, we obtained an exposure profile over 24,h for each of the participants. Exposure levels during waking hours were expressed as mean percentage of the reference level. Children with a low SES were more likely to own a mobile phone (OR 2.1; 95% CI: 1.1,3.9) and also reported to use their mobile phone longer per day (OR 2.4; 95% CI: 1.1,5.4) than children with a high SES. For adolescents, self-reported duration of mobile phone use per day was also higher with a low SES (OR: 3.4; 95% CI: 1.4,8.4) compared with a high SES. No association between SES and measured exposure to mobile telecommunication networks was seen for children or adolescents. Mobile phone use may differ between status groups with higher use among disadvantaged groups. However, this does not result in higher overall exposure to mobile telecommunication networks. Whether short duration of own mobile phone use or the small numbers of participants with a low SES are causal, have to be investigated in further studies. Bioelectromagnetics 31:20,27, 2010. © 2009 Wiley-Liss, Inc. [source]


Plasma sex steroid concentrations and gonadal aromatase activities in African clawed frogs (Xenopus laevis) from South Africa

ENVIRONMENTAL TOXICOLOGY & CHEMISTRY, Issue 8 2004
Markus Hecker
Abstract Adult African clawed frogs (Xenopus laevis) were collected from a corn-growing region (CGR) and a non-corn-growing region (NCGR) with different exposure profiles for atrazine and related triazines. Physical, chemical, and biological parameters from the catchment areas were also measured. Frogs were surveyed for possible effects of exposure to triazine herbicides on plasma testosterone (T) and estradiol (E2) titers, gonadal aromatase activity, and gonad growth (GSI). Concentrations of both T and E2 varied among locations and were correlated to some accessory factors, such as pH, several ions, and metals. Greatest median plasma T concentrations (males: 19 ng/ml; females: 16 ng/ml) occurred in frogs inhabiting NCGR as compared to those from the CGR (males: 4 ng/ml; females: 1 ng/ml). Median E2 concentrations were also greater in frogs collected from the NCGR (males: 3 ng/ml; females: 28 ng/ml) than those in frogs from the CGR (males: 2 ng/ml; females: 5 ng/ml). Because some exposure to agricultural chemicals at both regions occurred, as did simultaneous exposures to multiple chemicals, a regression analysis was employed. Negative correlations were observed between plasma T concentrations and concentrations of atrazine, deisopropylatrazine, deethylatrazine, and tertbuthylazine in females and between T and diaminochlorotriazine in males. Estradiol in females exhibited a significant negative correlation with atrazine and deethylatrazine. No correlations were observed between gonadal aromatase activity or GSI and any of the agricultural chemicals measured. Median aromatase activities in ovaries varied among sampling sites ranging from 7 to >3,000 times greater than those in males when measurable. Testicular aromatase activity was below the detection limit of the assay in male frogs at most of the sites. Although exposure to agricultural inputs did not affect aromatase activities, effects of atrazine or coapplied pesticides on sex steroid homeostasis cannot be excluded at this point. [source]


Association between asbestos exposure, cigarette smoking, myeloperoxidase (MPO) genotypes, and lung cancer risk

AMERICAN JOURNAL OF INDUSTRIAL MEDICINE, Issue 1 2002
Matthew B. Schabath MS
Abstract Background As observed in tobacco-associated carcinogenesis, genetic factors such as the polymorphic metabolic/oxidative enzyme myeloperoxidase (MPO) could modulate individual susceptibility to asbestos-associated carcinogenesis. Methods RFLP-PCR analysis identified the MPO genotypes in 375 Caucasian lung cancer cases and 378 matched controls. An epidemiological interview elicited detailed information regarding smoking history and occupational history and exposures. Results Asbestos exposure was associated with a significantly elevated risk estimate (OR,=,1.45; 95% CI 1.04,2.02). On stratified analysis, we found the MPO genotypes modified the effect of asbestos exposure on lung cancer risk. Specifically, G/G carriers who were exposed to asbestos had an odds ratio (OR) of 1.72 (95% CI; 1.09,2.66), while A-allele carriers (G/A,+,A/A) exposed to asbestos exhibited a reduced OR of 0.89 (95% CI; 0.56,1.44). The OR was further reduced to 0.73 (0.49,1.06) for A-allele carriers not exposed to asbestos. A similar trend was observed for the joint effects between the MPO genotypes and pack-years smoking. Next, all three risk factors (MPO genotypes, asbestos exposure, and smoking) were analyzed simultaneously for joint effects. Heavy smokers with the G/G genotype and a history of asbestos exposure demonstrated a statistically significant elevated risk estimate (OR,=,2.19; 95% CI 1.16,4.11), while the A-allele carriers with the same exposure profile were at a lower risk for lung cancer (OR,=,1.18; 95% CI 0.58,2.38). The A-allele genotypes demonstrated similar protective effects for the other three exposure profiles. Conclusions For a similar level of exposure to established carcinogens, individuals with the MPO A-allele genotypes appear to have a reduced risk of lung cancer. Am. J. Ind. Med. 42:29,37, 2002. © 2002 Wiley-Liss, Inc. [source]