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JournalISSN: 0048-7554

Reviews on environmental health 

De Gruyter
About: Reviews on environmental health is an academic journal published by De Gruyter. The journal publishes majorly in the area(s): Environmental exposure & Medicine. It has an ISSN identifier of 0048-7554. Over the lifetime, 1018 publications have been published receiving 24869 citations. The journal is also known as: Reviews on environmental health (Print).


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Journal ArticleDOI
TL;DR: An overview of the neurotoxic effects of lead with regard to children, adults, and experimental animals at both cellular and molecular levels is presented, and the biomarkers of lead exposure that are useful for risk assessment in the field of environmental health are discussed.
Abstract: Lead, a systemic toxicant affecting virtually every organ system, primarily affects the central nervous system, particularly the developing brain. Consequently, children are at a greater risk than adults of suffering from the neurotoxic effects of lead. To date, no safe lead-exposure threshold has been identified. The ability of lead to pass through the blood-brain barrier is due in large part to its ability to substitute for calcium ions. Within the brain, lead-induced damage in the prefrontal cerebral cortex, hippocampus, and cerebellum can lead to a variety of neurologic disorders. At the molecular level, lead interferes with the regulatory action of calcium on cell functions and disrupts many intracellular biological activities. Experimental studies have also shown that lead exposure may have genotoxic effects, especially in the brain, bone marrow, liver, and lung cells. Knowledge of the neurotoxicology of lead has advanced in recent decades due to new information on its toxic mechanisms and cellular specificity. This paper presents an overview, updated to January 2009, of the neurotoxic effects of lead with regard to children, adults, and experimental animals at both cellular and molecular levels, and discusses the biomarkers of lead exposure that are useful for risk assessment in the field of environmental health.

653 citations

Journal ArticleDOI
TL;DR: Examination of major uses and known toxic effects of commonly-used organohalogen flame retardants, replacements for those that have been phased out, their combustion by-products, and their effectiveness at reducing fire hazard concludes that flammability regulations can cause greater adverse environmental and health impacts than fire safety benefits.
Abstract: Since the 1970s, an increasing number of regulations have expanded the use of brominated and chlorinated flame retardants. Many of these chemicals are now recognized as global contaminants and are associated with adverse health effects in animals and humans, including endocrine and thyroid disruption, immunotoxicity, reproductive toxicity, cancer, and adverse effects on fetal and child development and neurologic function. Some flame retardants such as polybrominated diphenyl ethers (PBDEs) have been banned or voluntarily phased out by manufacturers because of their environmental persistence and toxicity, only to be replaced by other organohalogens of unknown toxicity. Despite restrictions on further production in some countries, consumer products previously treated with banned retardants are still in use and continue to release toxic chemicals into the environment, and the worldwide use of organohalogen retardants continues to increase. This paper examines major uses and known toxic effects of commonly-used organohalogen flame retardants, replacements for those that have been phased out, their combustion by-products, and their effectiveness at reducing fire hazard. Policy and other solutions to maintain fire safety while reducing toxicity are suggested. The major conclusions are: (1) Flammability regulations can cause greater adverse environmental and health impacts than fire safety benefits. (2) The current options for end-of-life disposal of products treated with organohalogens retardants are problematic. (3) Life-cycle analyses evaluating benefits and risks should consider the health and environmental effects of the chemicals, as well as their fire safety impacts. (4) Most fire deaths and most fire injuries result from inhaling carbon monoxide, irritant gases, and soot. The incorporation of organohalogens can increase the yield of these toxic by-products during combustion. (5) Fire-safe cigarettes, fire-safe candles, child-resistant lighters, sprinklers, and smoke detectors can prevent fires without the potential adverse effects of flame retardant chemicals. (6) Alternatives to organohalogen flame retardant chemicals include using less flammable materials, design changes, and safer chemicals. To date, before evaluating their health and environmental impacts, many flame retardant chemicals have been produced and used, resulting in high levels of human exposure. As a growing literature continues to find adverse impacts from such chemicals, a more systematic approach to their regulation is needed. Before implementing new flammability standards, decision-makers should evaluate the potential fire safety benefit versus the health and environmental impacts of the chemicals, materials, or technologies likely to be used to meet the standard. Reducing the use of toxic or untested flame retardant chemicals in consumer products can protect human and animal health and the global environment without compromising fire safety.

425 citations

Journal ArticleDOI
TL;DR: The polychlorinated biphenyls are synthetic organochlorine chemicals that were useful industrial products in the past, but their production was ended because they persist in both the environment and living organisms.
Abstract: The polychlorinated biphenyls (PCBs) are synthetic organochlorine chemicals that were useful industrial products in the past, but their production was ended because they persist in both the environment and living organisms. The PCBs are mixtures of up to 209 different components (congeners), depending on the number and position of chlorines around the biphenyl ring. The PCBs are fat-soluble substances to which everyone is exposed through ingesting animal fats, inhalation, or dermal contact. Exposure to PCBs suppresses the immune system, thereby increasing the risk of acquiring several human diseases. Both ortho-substituted and coplanar (dioxin-like) congeners are tumor promoters that enhance the effects of other carcinogenic substances. PCB exposure, especially during fetal and early life, reduces IQ and alters behavior. The PCBs alter thyroid and reproductive function in both males and females and increase the risk of developing cardiovascular and liver disease and diabetes. Women are at high risk of giving birth to infants of low birth weight, who are at high lifetime risk for several diseases. As knowledge of their toxic effects has grown faster than environmental levels have declined, PCBs remain dangerous contaminants.

397 citations

Journal ArticleDOI
TL;DR: The nature of such damage, the cellular conditions in which it occurs, and oxidative-stress data that may be applied to the development of risk-assessment methods and models that are designed to reduce some of these uncertainties are reviewed.
Abstract: Pesticide-induced oxidative stress as a possible mechanism of toxicity has been a focus of toxicological research for the last decade. Yet for certain pesticides, mechanisms leading to oxidative stress are only partly understood. Pesticide-induced oxidative stress is the final manifestation of a multi-step pathway, resulting in an imbalance between pro-oxidant and antioxidant defense mechanisms. Concomitantly, pesticide intoxication induces a derangement of certain antioxidant mechanisms in different tissues, including alterations in antioxidant enzymes and the glutathione redox system. In this article, we discuss the impact of certain factors that are important in the potentiation of pesticide-induced oxidative stress, immunotoxicity, and apoptosis. Understanding risk factors largely depends upon the cellular and molecular events underlying pesticide-induced stress in experimental animals. These factors must be considered in the safety/toxicity evaluation of any pesticide. The identification and characterization of plant products/drugs might be helpful for understanding the mechanisms of compensation and repair that are due to oxidative stress-induced injury. This paper reviews the nature of such damage, the cellular conditions in which it occurs, and oxidative-stress data that may be applied to the development of risk-assessment methods and models that are designed to reduce some of these uncertainties.

377 citations

Journal ArticleDOI
TL;DR: Suggestive evidence was found that exposure to PM2.5 is positively associated with mortality from coronary heart diseases and exposure to SO2 increases mortality from lung cancer and for the other pollutants and health outcomes, the data were insufficient to make solid conclusions.
Abstract: We conducted a systematic review of all studies published between 1950 and 2007 of associations between long-term exposure to ambient air pollution and the risks in adults of nonaccidental mortality and the incidence and mortality from cancer and cardiovascular and respiratory diseases. We searched bibliographic databases for cohort and case-control studies, abstracted characteristics of their design and conduct, and synthesized the quantitative findings in tabular and graphic form. We assessed heterogeneity, estimated pooled effects for specific pollutants, and conducted sensitivity analyses according to selected characteristics of the studies. Our analysis showed that long-term exposure to PM2.5 increases the risk of nonaccidental mortality by 6% per a 10 microg/m3 increase, independent of age, gender, and geographic region. Exposure to PM2.5 was also associated with an increased risk of mortality from lung cancer (range: 15% to 21% per a 10 microg/m3 increase) and total cardiovascular mortality (range: 12% to 14% per a 10 microg/m3 increase). In addition, living close to busy traffic appears to be associated with elevated risks of these three outcomes. Suggestive evidence was found that exposure to PM2.5 is positively associated with mortality from coronary heart diseases and exposure to SO2 increases mortality from lung cancer. For the other pollutants and health outcomes, the data were insufficient data to make solid conclusions.

353 citations

Performance
Metrics
No. of papers from the Journal in previous years
YearPapers
202329
202284
202193
202054
201943
201835