Archive for the ‘Environmental Toxicants’ Category

Low level of exposure to pesticides leads to lung dysfunction in occupationally exposed subjects.

Tuesday, February 10th, 2009

Inhal Toxicol. 2008 Jul;20(9):839-49. Links

Low level of exposure to pesticides leads to lung dysfunction in occupationally exposed subjects.
Hernández AF, Casado I, Pena G, Gil F, Villanueva E, Pla A.

Department of Legal Medicine and Toxicology, University of Granada Medical School, Granada, Spain. ajerez@ugr.es

Pesticides may contribute to adverse respiratory health effects among farmers and have been considered one causal factor for the rise in asthma prevalence. This cross-sectional study was conducted to evaluate potential respiratory function abnormalities following long-term pesticide exposure by means of a complete pulmonary function testing, including spirometry, lung volumes, and diffusing capacity for carbon monoxide. The study population was comprised by workers from a prominent intensive agriculture area of southern Spain that relied on pesticides for the control of plagues. Eighty-nine pesticide sprayers of plastic greenhouse farming and a control group of 25 nonspraying control farmers from the same area were interviewed by a general practitioner asking about sociodemographic factors, occupational exposure, and clinical symptoms by using a structured questionnaire. Multiple regression analyses showed a relationship of short-term exposure to pesticides (as indicated by a drop in serum cholinesterase > 25% of baseline levels) with reduced forced expired volume in 1 s, and of long-term exposure (as indicated by a cumulative pesticide exposure index) with reduced forced expiratory flow rate. Exposure to bipyridilium-class herbicides was a determinant of a fall in the diffusing capacity of the lungs, and neonicotinoid insecticides showed a relationship with lower pulmonary volumes (total lung capacity, residual volume, and functional residual capacity), suggestive of restrictive lung disease, and with an increased risk of reporting irritative symptoms.

PMID: 18645724 [PubMed - indexed for MEDLINE] Inhal Toxicol. 2008 Jul;20(9):839-49. Links

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Environmental exposures and gene regulation in disease etiology.

Tuesday, February 10th, 2009

Cien Saude Colet. 2008 Jan-Feb;13(1):269-81.

Environmental exposures and gene regulation in disease etiology.
Edwards TM, Myers JP.

Department of Zoology, University of Florida, Gainesville, FL 32611, USA. tedwards@zoo.ufl.edu

Health or disease is shaped for all individuals by interactions between their genes and environment. Exactly how the environment changes gene expression and how this can lead to disease are being explored in a fruitful new approach to environmental health research, representative studies of which are reviewed here. We searched Web of Science and references of relevant publications to understand the diversity of gene regulatory mechanisms affected by environmental exposures with disease implications. Pharmaceuticals, pesticides, air pollutants, industrial chemicals, heavy metals, hormones, nutrition, and behavior can change gene expression through a broad array of gene regulatory mechanisms. Furthermore, chemically induced changes in gene regulation are associated with serious and complex human diseases, including cancer, diabetes and obesity, infertility, respiratory diseases, allergies, and neurodegenerative disorders such as Parkinson and Alzheimer diseases. The reviewed studies indicate that genetic predisposition for disease is best predicted in the context of environmental exposures. And the genetic mechanisms investigated in these studies offer new avenues for risk assessment research. Finally, we are likely to witness dramatic improvements in human health, and reductions in medical costs, if environmental pollution is decreased.

PMID: 18813540 [PubMed - in process]
http://www.ncbi.nlm.nih.gov/pubmed/18813540?dopt=AbstractPlus

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Inter-individual susceptibility to environmental toxicants–a current assessment

Friday, February 6th, 2009

Inter-individual susceptibility to environmental toxicants–a current assessment

Nebert DW.

Department of Environmental Health, Center for Environmental Genetics, University of Cincinnati Medical Center, P.O. Box 670056, Cincinnati, OH 45267-0056, USA. dan.nebert@uc.edu

Toxicol Appl Pharmacol. 2005 Sep 1;207(2 Suppl):34-42

Virtually all diseases have an environmental component. The two most important factors affecting your unique risk of an environmental disease (toxicity or cancer) are (a) your exposure to the environmental agent and (b) your genes. Epidemiologists have found ways to calculate inter-individual risk–if the exposure to environmental agents is sufficiently high and can be documented (e.g., years of cigarette smoking, taking prescribed drugs, drinking alcohol, or exposure to radon or other radioactive material, etc.). If the dose of environmental agents is lower and more ambiguous (e.g., exposure to chemicals on the job, herbicides sprayed on a golf course, outdoor or indoor air pollution, endocrine disruptors in cans of food, living near a toxic waste dump site, etc.), however, calculations of inter-individual risk become much more difficult. Highly accurate DNA tests for genetic susceptibility to toxicity and cancer have been sought in order to identify individuals at increa sed risk; this type of research represents the leading edge of phenotype-genotype association studies and is the major goal of most public health and preventive medicine programs. The task, however, has turned out to be far more challenging than anticipated. The major stumbling block has been the difficulty in determining an unequivocal phenotype or an unequivocal genotype. We were quite optimistic 5-10 years ago that this would be easy, but now we are beginning to appreciate how difficult it is to determine an unequivocal phenotype or genotype with certainty. For many reasons set forth in this overview, it appears that DNA testing alone, to predict and prevent environmental disease on an individual basis, may be virtually impossible with current knowledge and technologies and will require novel insights before major practical applications will evolve.

http://www.ncbi.nlm.nih.gov/pubmed/15982695?dopt=AbstractPlus

PMID: 15982695 [PubMed - indexed for MEDLINE]

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