Explore the vast range of titles available.

The politics and science of health and disease remain contested terrain among scientists, health practitioners, policy makers, industry, communities, and the public. Stakeholders in disputes about illnesses or conditions disagree over their fundamental causes as well as how they should be treated and prevented. This thought-provoking book crosses disciplinary boundaries by engaging with both public health policy and social science, asserting that science, activism, and policy are not separate issues and showing how the contribution of environmental factors in disease is often overlooked.

This chapter contains sections titled: Introduction Disease Ecology and Environment Discussion: Towards Vulnerable Places Conclusion References

Children with complex congenital heart disease are less active than recommended for optimal health, with social and physical environments important determinants. The purpose of this study was to examine the physical activity perceptions of children with complex congenital heart disease and their parents to identify social and physical environment intervention targets. A semi-structured discussion guide elicited physical activity perceptions from children (26 boys, 19 girls, 6.0–12.4 years) with complex congenital heart disease (single ventricle n = 42) and their parents during three child and three parent focus groups and 41 interviews. Interviews and focus groups were audio-recorded and transcribed verbatim for inductive thematic analysis. Children and parents identified home, peer and health environments as impacting on their children’s physical activity participation. Peer environments, such as school or daycare, were supportive by providing physical activity facilities and enabling fun with peers and time outdoors. At home, parent and sibling interactions both encouraged and discouraged physical activity. The children’s unique health environment fostered physical activity uncertainty, discouraging activity despite minimal or no physician recommendations to restrict physical activity. Children with complex congenital heart disease and their parents recognize the importance of physical activity and fun with friends. Physical activity uncertainty contributes to their inactive lifestyles despite minimal restrictions from health professionals. Positive clinical encouragement and health environment interventions that better support physical activity are required.

This review paper investigates a specific environmental-disease interaction between mercury exposure and Alzheimer’s disease hallmarks. Alzheimer’s disease is a neurodegenerative disorder affecting predominantly the memory of the affected individual. It prevails mostly in the elderly, rendering many factors as possible causative agents, which potentially contribute to the disease pathogenicity cumulatively. Alzheimer’s disease affects nearly 50 million people worldwide and is considered one the most devastating diseases not only for the patient, but also for their families and caregivers. Mercury is a common environmental toxin, found in the atmosphere mostly due to human activity, such as coal burning for heating and cooking. Natural release of mercury into the atmosphere occurs by volcanic eruptions, in the form of vapor, or weathering rocks. The most toxic form of mercury to humans is methylmercury, to which humans are exposed to by ingestion of fish. Methylmercury was found to exert its toxic effects on different parts of the human body, with predominance on the brain. There is no safe concentration for mercury in the atmosphere, even trace amounts can elicit harm to humans in the long term. Mercury’s effect on Alzheimer’s disease hallmarks formation, extracellular senile plaques and intracellular neurofibrillary tangles, has been widely studied. This review demonstrates the involvement of mercury, in its different forms, in the pathway of amyloid beta deposition and tau tangles formation. It aims to understand the link between mercury exposure and Alzheimer’s disease so that, in the future, prevention strategies can be applied to halt the progression of this disease.

STUDY OBJECTIVE--The aim was to estimate the quantitative impact of working conditions on cardiovascular diseases in Denmark. DESIGN--The study was based on a review of recent epidemiological research publications in which relative risks were estimated and risk factor prevalences were determined. The impact of working conditions was quantified by means of aetiological fractions. SETTING--The aetiological fractions were estimated on the Danish population. MAIN RESULTS--16% of the premature cardiovascular mortality in men and 22% in occupationally active women is avoidable through interventions in the work environment. If \"sedentary\" work is included in the occupational risk factors, the aetiological fractions reach 51% for men and 55% for women. Taken separately, the major aetiological fractions for cardiovascular risk factors at work are respectively (women in parentheses) 6% (14%) for monotonous high paced work, 7% (7%) for shift work, and 2% (2%) for passive smoking. CONCLUSIONS--The aetiological fractions show that working conditions play a considerable role in cardiovascular diseases. Furthermore they might widen the focus of preventive cardiology from interventions directed only at individual and lifestyle risk factors to interventions directed also at working conditions.

This chapter contains sections titled: Introduction How Vectors Move Summary References

STUDY OBJECTIVE--The aim was to identify socioeconomic variables associated with deaths and hospital admissions due to hypothermia and to quantify the risk due to ambient outside temperature. DESIGN--The study was a survey of deaths and hospital admissions due to hypothermia (ICD 991.6), for the period 1979-85 inclusive, identified from death certificates and Hospital Inpatient Enquiry (HIPE) data. SETTING--The study included all deaths and hospital admissions due to hypothermia (1979-85) in the 26 counties of the Republic of Ireland, population 3.5 million. SUBJECTS--All deaths coded during the study period as being due to hypothermia and all persons admitted to hospital during the study period for whom hypothermia was recorded as a discharge diagnosis in HIPE data. MEASUREMENTS AND MAIN RESULTS--Demographic data and date of death/diagnosis were obtained from both data sets. Complete national temperature records were obtained from the meteorological service and a temperature was assigned to each case representing ambient outside temperature at which hypothermia developed. Risk of hypothermia at a given temperature was obtained by dividing the number of cases at that temperature by the appropriate person-years of exposure of the entire national population. Incidence of and mortality from hypothermia doubled with each 5 degrees C and 4 degrees C fall in temperature respectively; the majority of deaths and hospital admissions occurred between October and March. Incidence and mortality increased with age and men had 30% higher case fatality than women. Single men had four times the incidence and 6.5 times the mortality, and single women had double the incidence and four times the mortality of married men and women respectively. Low population density was also an important risk marker. CONCLUSIONS--The risk of hypothermia due to ambient outside temperature has been quantified and a high risk group was identified. A combination of statutory support measures and good neighbourliness could prevent illness and deaths from hypothermia.

Parkinson’s disease (PD) affects millions around the world. The Braak hypothesis proposes that in PD a pathologic agent may penetrate the nervous system via the olfactory bulb, gut, or both and spreads throughout the nervous system. The agent is unknown, but several environmental exposures have been associated with PD. Here, we summarize and examine the evidence for such environmental exposures. We completed a comprehensive review of human epidemiologic studies of pesticides, selected industrial compounds, and metals and their association with PD in PubMed and Google Scholar until April 2016. Most studies show that rotenone and paraquat are linked to increased PD risk and PD-like neuropathology. Organochlorines have also been linked to PD in human and laboratory studies. Organophosphates and pyrethroids have limited but suggestive human and animal data linked to PD. Iron has been found to be elevated in PD brain tissue but the pathophysiological link is unclear. PD due to manganese has not been demonstrated, though a parkinsonian syndrome associated with manganese is well-documented. Overall, the evidence linking paraquat, rotenone, and organochlorines with PD appears strong; however, organophosphates, pyrethroids, and polychlorinated biphenyls require further study. The studies related to metals do not support an association with PD.

STUDY OBJECTIVE--The aim was to investigate the association between mothers' occupational exposure during pregnancy and the incidence of acute lymphoblastic leukaemia in children. DESIGN--The study was a case-control investigation. A face to face interview was used to assess exposures at work and relevant confounding variables. SETTING--The study was community based and was carried out in five provinces of Spain. SUBJECTS--128 cases less than 15 years of age were interviewed (91% of those eligible). Controls (one for each case) were chosen from the census lists and were matched on year of birth, sex and municipality. MEASUREMENTS AND MAIN RESULTS--Children of mothers working at home had a relative risk (RR) of 7.0 (95% CI = 1.59-30.79) of developing acute lymphoblastic leukaemia. Exposure to organic dust was associated with a RR of 5.5 (95% CI = 1.21-24.8). There was a statistically significant interaction between exposure to organic dust and working at home. The majority of women working at home were hired by local industries to sew different types of tissues (cotton, wool, synthetic fibres) on a machine. CONCLUSION--A similar association has not been reported before: if confirmed, this finding may suggest a new health concern.

STUDY OBJECTIVE--The aim was to investigate the relationship between social factors and stroke mortality in men and women aged between 45 and 74 years using census and mortality data from 32 London boroughs in 1971 and 1981. DESIGN--Census data from 1971 and 1981 on type of accommodation, density of room occupation, male unemployment rate, and proportion of households without a car were linked with stroke mortality available for each London borough. SETTING--32 London boroughs excluding the City of London. MEASUREMENTS AND MAIN RESULTS--The main outcome measures were the association between age adjusted mortality from stroke and the proportion of households with no car, non-ownership of home, in council housing or rented accommodation, male unemployment rate, and living density of more than 1.5 people per room. There was no strong correlation between social variables and stroke mortality in 1971, but strong correlations were found for male stroke mortality in 1981. The highest correlation was with male unemployment (r = 0.64, p less than 0.001) even after adjusting for the proportion of the population born in the Caribbean and Africa (r = 0.56, p less than 0.01). Other social variables were also highly correlated with male stroke mortality: households without a car (r = 0.63, p less than 0.001), living density of more than 1.5 people per room (r = 0.053, p less than 0.001), council housing (r = 0.45, p = 0.01), and rented accommodation (r = 0.36, p = 0.05). After regressing male mortality on unemployment rate the other social variables were no longer significantly correlated with male stroke mortality. In women, the only significant correlation was found in 1981 between stroke mortality and the proportion of families living in council housing (r = 0.34, p = 0.05). CONCLUSIONS--Social factors are important indicators of stroke mortality. The major increases in unemployment over the decade may explain the generally stronger association in 1981 compared with 1971. Male stroke mortality increased by 0.062/1000 for every one percent increase in male unemployment (0.054/1000 after adjusting for place of birth).