Related Adverse Health Effects Research Articles

International Perspectives

Consanguinity is defined as the marriage between individuals who have a common ancestor. Many epidemiologic studies have examined consanguineous marriages and their health impact on offspring. Because related individuals share genes from a common ancestor, homozygosity is favored, and their progeny are more likely to have genetic disorders. Primarily, offspring of consanguineous parents are at a twofold greater risk than offspring of nonrelated parents for autosomal recessive disorders. (1)(2) Advances in genetics have led to a deeper understanding of the impact of inbreeding on the occurrence of genetic anomalies. Studies show that inbreeding is associated with mortality and morbidity in the fetal, neonatal, and childhood stages. Because consanguinity represents a risk factor for the occurrence of many deleterious outcomes, it is of major scientific and public health interest. This article summarizes the primary health-related adverse effects of consanguinity and discusses potential preventive measures. Despite the adverse effects caused by consanguineous unions, such relationships still occur in many countries. Bittles (3) has illustrated the global prevalence of consanguineous marriage (Fig. 1). The prevalence can be divided into three major regions. The first region includes Western Europe, North America, Australasia, and Russia, where only 1% of marriages are consanguineous. The second region includes the Iberian Peninsula, Japan, and South America, where 1% to 10% of marriages are consanguineous. The third region includes most of North and sub-Saharan Africa as well as West, Central and South Asia, where 20% to 50% of marriages are consanguineous. The specific types and rate of consanguineous marriages vary between and within countries. In the Middle East, the overall rate of consanguineous unions varies between 21% in Lebanon (Ministry of Public Health, 1998) and up to 58% in Saudi Arabia. (4) The most common form of consanguineous unions practiced is between first cousins. The rate of …

A Killer Smell: Mold Toxin Destroys Olfactory Cells in Mice

Mold seems ubiquitous: it permeates spaces made damp by leaking water lines, faulty roofs, or storm flooding. Although no one contests that its slimy presence is a general nuisance, its related adverse health effects have been the subject of some controversy. Now researchers at Michigan State University’s Center for Integrative Toxicology have found that a toxin produced by the black mold Stachybotrys chartarum can damage nerve cells key to the sense of smell, at least in the noses of mice [EHP 114:1099–1107; Islam et al.]. The study is the first to probe how inhaling black mold toxins affects nasal passages. Other researchers have previously reported links between S. chartarum exposure and human health effects including upper and lower respiratory illnesses. There is also evidence of an association between exposure to fungi in a damp indoor environment and effects such as asthma symptoms in sensitive individuals. However, in a recent Institute of Medicine report, a panel of experts concluded that there is limited or insufficient evidence to determine whether an association exists for other suggested health outcomes such as chronic obstructive pulmonary disease, neuropsychiatric symptoms, skin symptoms, and immune diseases. The Michigan team found that a single low dose of satratoxin G administered directly into the noses of mice selectively killed sensory neurons involved in detecting odors and sending signals to the olfactory bulbs in the brain. Satratoxins are a type of mycotoxin found in the spores and other parts of S. chartarum. The toxins killed the olfactory neurons by apoptosis while apparently leaving bystander cells unharmed. The mice that inhaled the fungal toxins also developed inflammation of the nasal passages and rhinitis (“runny nose” symptoms), as well as milder inflammation of the olfactory bulbs. It is still unclear how these findings apply to humans exposed to molds. Moreover, before broader health impacts may be assessed, both the amounts of mycotoxins in the air and the nature of human exposure need to be better understood, as do the effects of mold toxins on humans’ sense of smell and nasal inflammation. On first examination, however, these mouse studies suggest that exposure to airborne mold toxins may adversely affect people’s ability to smell. At a minimum, the study raises new questions about the hazards of exposure to black mold in water-damaged buildings.

The occupational toxicologist: professionalism, morality and ethical standards in the context of legal and non-litigation issues

By its very nature, practice and intended applications, the profession of occupational toxicology has individual and collective responsibilities related to the design, conduct, interpretation and extrapolation of laboratory and controlled human clinical studies in order to determine the potential for industrial xenobiotics to produce adverse effects. The implications for health-related adverse effects in the workplace, and in the domestic and general environment carries many and various responsibilities for the toxicologist which are related to multiple and wide-ranging ethical issues. This review presents and discusses some of the major areas where the occupational toxicologist may experience potential ethical problems related to the conduct of routine professional activities. Emphasis is placed on the design, conduct, interpretation and reporting of laboratory studies; animal welfare; regulatory activities; human clinical volunteer studies; roles and responsibilities in defining workplace safety and protective measures; malpractices in various disciplines and work practices; misconduct in publication; and codes of ethical behavior.

Chronic health effects in people exposed to arsenic via the drinking water: dose–response relationships in review

Chronic arsenic (As) poisoning has become a worldwide public health issue. Most human As exposure occurs from consumption of drinking water containing high amounts of inorganic As (iAs). In this paper, epidemiological studies conducted on the dose–response relationships between iAs exposure via the drinking water and related adverse health effects are reviewed. Before the review, the methods for evaluation of the individual As exposure are summarized and classified into two types, that is, the methods depending on As concentration of the drinking water and the methods depending on biological monitoring for As exposure; certain methods may be applied as optimum As exposure indexes to study dose–response relationship based on various As exposure situation. Chronic effects of iAs exposure via drinking water include skin lesions, neurological effects, hypertension, peripheral vascular disease, cardiovascular disease, respiratory disease, diabetes mellitus, and malignancies including skin cancer. The skin is quite sensitive to arsenic, and skin lesions are some of the most common and earliest nonmalignant effects related to chronic As exposure. The increase of prevalence in the skin lesions has been observed even at the exposure levels in the range of 0.005–0.01 mg/l As in drinking waters. Skin, lung, bladder, kidney, liver, and uterus are considered as sites As-induced malignancies, and the skin is though to be perhaps the most sensitive site. Prospective studies in large area of endemic As poisoning, like Bangladesh or China, where the rate of malignancies is expected to increase within the next several decades, will help to clarify the dose–response relationship between As exposure levels and adverse health effects with enhanced accuracy.

Prevalence of overweight and obesity for urban adults in Cameroon

Background: The emergence of a nutrition transition in developing countries might lead to higher prevalence of obesity and related adverse health effects. In Cameroon, urbanization growth rate is one of the highest in sub-Saharan Africa. Such dramatic demographic change favours important modifications, notably in nutritional patterns. Aim: In this paper we examine the current prevalence of overweight and obesity in Yaoundé, the capital city of Cameroon and search for possible causal factors. Detrimental consequences of overweight are also discussed. Material and methods: Samples of adults (519 women, 252 men) of all ages in all districts of Yaoundé were subjected to anthropometric and body composition measurements, blood pressure and resting heart rate determination, and interviewer-administered questionnaires on socio-demography, smoking habits, physical activity, self-perception of body weight and health status. Results: In both sexes body mass index (BMI) increases with age and peaks in the years of maturity. These changes are related to changes in adiposity. Prevalence rates of overweight (BMI ≥ 25) and obesity (BMI ≥ 30) increase from 20 to 29 years and peak at 40-49 years in men and at 50-59 years in women before starting to decline. One woman in two is overweight and one woman in five is obese, whereas one-third of men are overweight and only 5% are obese. Obese subjects have a larger age-adjusted waist to hip ratio (WHR) than their non-overweight counterparts, attesting that fat gain is oriented towards a more abdominal fat mass distribution. The length of residence in Yaoundé, increasing education level, occupation, ethnicity, physical inactivity and smoking practices appear to influence early overweight and/or obesity. No parity effect is observed in women. From the present study, it appears that obesity, and especially obesity in women, could be less benign than that described in other studies in Africa. Conclusion: Research is needed in Cameroon, including aetiological and cohort studies aimed at the quantification of morbidity and mortality risks associated with overweight and obesity.

Tests for Biologic Markers of Genotoxic Exposure and Effect

Markers of genetic damage are being used increasingly to under- stand and prevent environmentally related human adverse health effects. A major example has been the application of such markers to the prediction of chemical carcinogenicity. Over the past 15 years, hundreds of test systems in microorganisms, cell cultures and animals were devised and applied to this end. In spite of early successes, recent results show a discouragingly low, 60% agreement between the genetic tests and conventional, whole animal, long-term carcinogenicity assays. Corresponding efforts to predict the heritable mutagenicity of chemicals using genetic tests that do not involve heritability have given similar results. New technologic developments for the first time are letting us make such genotoxicity measurements directly in human subjects. Examples include detection of DNA adducts, measurement of somatic mutations and improved cytogenetic methods. There is also the possibility of soon finding sufficiently sensitive methods to estimate heritable mutagenicity as a predictor of damage to future generations. These biologic markers of genotoxicity are useful for estimating human exposure and effect, for identifying toxic environments, for monitoring cancer chemotherapy and for identifying susceptible populations. They offer a major new challenge to epidemiology and public health.

Interpreting pesticide residue data at the analytical level.

The natures, locations, and quantities of pesticide residues in foodstuffs are important in the realm of the public health; these residues in animal feeds are important, also, in animal husbandry, for they conceivably could affect the health and well-being of the animal as well as of the ultimate consuming public through possibly pesticide-contaminated edible animal products. Properly used under the now legalized aegis in many countries of “good agricultural practice,” with all the constraints attached thereto, there should be no nutritional or other health-related adverse effects from pesticide or pesticide-derived residues persisting in the agricultural environment. It is the occasional misuse or illegal use of pesticide chemicals,1 however, which could result in possibly deleterious residues persisting from attempted pest-control applications into human foodstuffs or animal feeds. It is not the intent here to dwell on the many complications that can result from over-contamination with pesticide chemicals of the nonedible agricultural environment such as soil, runoff and other initially agricultural waters, nontarget plants, wild animal and aquatic life, and air.