RESUMO
Sustenance of smallholder poultry production as an alternative source of food security and income is imperative in communities exposed to hydrocarbon pollution. Exposure to hydrocarbon pollutants causes disruption of homeostasis, thereby compromising the genetic potential of the birds. Oxidative stress-mediated dysfunction of the cellular membrane is a contributing factor in the mechanism of hydrocarbon toxicity. Epidemiological studies show that tolerance to hydrocarbon exposure may be caused by the activation of genes that control disease defense pathways like aryl hydrocarbon receptor (AhR) and nuclear factor erythroid 2p45-related factor 2 (Nrf2). Disparity in the mechanism and level of tolerance to hydrocarbon fragments among species may exist and may result in variations in gene expression within individuals of the same species upon exposure. Genomic variability is critical for adaptation and serves as a survival mechanism in response to environmental pollutants. Understanding the interplay of diverse genetic mechanisms in relation to environmental influences is important for exploiting the differences in various genetic variants. Protection against pollutant-induced physiological responses using dietary antioxidants can mitigate homeostasis disruptions. Such intervention may initiate epigenetic modulation relevant to gene expression of hydrocarbon tolerance, enhancing productivity, and possibly future development of hydrocarbon-tolerant breeds.
RESUMO
The implications of environmental contamination on human health in the Niger Delta region of Nigeria remain a topic of growing international public health interest. To better understand ongoing air pollution and initiate remediation efforts, the United Nations Environmental Programme (UNEP) report recommended the monitoring of volatile organic compounds (VOCs) across different media (water, soil, and air) in Ogoniland, an at-risk population in the Niger Delta region of Nigeria. In this pilot study, we measured indoor VOC concentrations in the indoor air of 20 households in Ogale, an Ogoniland community whose groundwater system is contaminated with benzene at levels 900 times the World Health Organization guidelines and evaluated self-reported health conditions and predicted cancer risks and hazards from inhalation exposure to VOCs. We detected higher concentrations of benzene (mean = 25.7 µg/m³, SD = 23.2 µg/m³) and naphthalene (mean = 7.6 µg/m³, SD = 13.8 µg/m³) than has been reported in other regions. Although study participants reported health symptoms consistent with VOC exposure, we were underpowered to detect a significant association between select indoor VOCs and these self-reported health symptoms using univariate logistic regression models. These findings suggest that that the health symptoms reported by participants may be poor proxies for the underlying disease processes associated with adverse health outcomes due to VOC exposure in this community and that the burden of adverse health effects due to VOC exposure may stem from the contaminated groundwater system. We estimated a non-cancer hazard quotient of 3 from exposure to naphthalene and lifetime excess cancer risks from exposure to naphthalene, benzene, p-dichlorobenzene, carbon tetrachloride, and ethylbenzene of 3 × 10-4, 2 × 10-4, 6 × 10-5, 6 × 10-6, and 1 × 10-5, respectively. These results exceed common risk benchmarks in the United States, suggesting a need for further studies to characterize VOC exposures, sources, and associated health risks in the Niger Delta.
