Air pollution: What is it and what we must do.

There is widespread misunderstanding of air pollution and its effects in the media. This relates to the complexities of studying and reporting on the issue - multiple different associated pollutants and diverse reported toxic effects. This article explains what air pollution is and how it may affect health, from heart to brain. It then explains, using Scotland as an example, how pollution can be reduced to levels at which public health effects become small but that, because of its close causative link with climate change, both government action and, especially, our individual responses to the issue are still urgently necessary. The medical profession is urged to set an example by reducing personal carbon footprints.

The recognition of lung disease in coal workers: The role of Gough-Wentworth whole lung sections.

From the identification of a specific lung disease caused by coal dust exposure in miners in 1831 until the demonstration of the association of that exposure to risk of emphysema in 1984, there was continuous argument about the harmfulness of coal dust. Ill health in miners was attributed variously to tuberculosis, quartz exposure or cigarette smoking. An acceptance that coal dust was harmful only started with investigative radiology and pathology in the 1920s, and physiology in the 1950s. Most of the early investigations were in South Wales, the centre of the most important coal field in Great Britain. Among the investigators was Professor Jethro Gough who, with his technician James Wentworth, introduced a technique for making thick sections of whole, inflated lungs on paper backing. Here, we describe this method and its central role in understanding the relationships between coal dust exposure, pneumoconiosis, emphysema and lung dysfunction in miners.

Science With Purpose: 50 Years of the Institute of Occupational Medicine.

The Institute of Occupational Medicine (IOM) was founded in 1969 by the then UK National Coal Board to complete its nation-wide epidemiological study of lung disease in coal miners, the Pneumoconiosis Field Research. The results quantified risks in the industry and were influential across the world in setting preventive standards. The research, based on epidemiology, was multidisciplinary from the start, and the IOM's broad scientific expertise was applied across many other industries with an increasing focus on environmental measurement and ergonomics. In 1990, as the coal industry declined, IOM became a self-funding research charity with a strong commercial arm. It has expanded its research, often with European collaborators and funding from governments, and has achieved wide recognition. This has most recently been applied during the pandemic in areas of hospital ventilation, personal protection, and viral exposure research, illustrating IOM's ability to respond to new environmental or occupational challenges.

Caring for the Carers of COVID-19.

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Pollution, Particles, and Dementia: A Hypothetical Causative Pathway.

Epidemiological studies of air pollution have shown associations between exposure to particles and dementia. The mechanism of this is unclear. As these seem unlikely in terms of the very small dose likely to reach the brain in usual Western urban circumstances, we extend our 1995 hypothetical explanation of the association of air pollution with cardiac deaths as a plausible alternative explanation of its associations with dementia. Since our original proposal, it has become apparent that inflammation may be carried by blood from organ to organ by biologic microparticles derived from cell membranes. These transmit inflammatory messages to endothelial cells throughout the body as part of a general defensive response to assumed bacterial infection; particulate air pollution has recently been shown to be associated with their release into the blood. We propose that episodic release of biologic microparticles from pollution-induced lung inflammation causes secondary inflammation in the blood-brain barrier and cerebral microbleeds, culminating over time in cognitive impairment. Ultimately, by incomplete repair and accumulation of amyloid, this increases the risk of Alzheimer's disease. Importantly, this mechanism may also explain the relationships of other inflammatory conditions and environmental factors with cognitive decline, and point to new opportunities to understand and prevent dementia.

Black lungs in the general population: a new look at an old dispute.

Almost from the time that autopsies were first routinely carried out, darkening of lungs with increasing age was described. Different explanations for the origin of the accumulating black pigment arose and by the early nineteenth century three hypotheses had emerged: 1) soot inhaled into the lungs from the air; 2) carbon accumulating in the lungs from abnormal pulmonary carbon dioxide metabolism; and, 3) pigment derived from the blood. In 1813 the English physician and chemist George Pearson published a paper in which he described the recovery of the black pigment from lungs and its chemical analysis. Pearson declared the black pigment to be airborne carbon/soot from the burning of coal and wood. He described these particles depositing in 'black spots' in the terminal airways and accumulating in the peribronchial lymph nodes, forming 'black glands'. Despite Pearson's prescient account, debate continued and the true explanation, given in that paper, was not fully accepted until the late nineteenth century.

Maternal vitamin D and E intakes in pregnancy and asthma to age 15 years: A cohort study.

This study investigated whether the previously reported associations in this birth cohort between maternal vitamin D and E intakes during pregnancy and childhood wheeze/asthma outcomes at age 5 and 10 years are still evident at age 15 years. In a prospective study of 1924 children recruited in utero, maternal vitamin D and E intakes during pregnancy were assessed by food frequency questionnaire and the children completed raespiratory questionnaire at age 15 years. Treatment for asthma at age 15 was also ascertained using healthcare data. Maternal vitamin D and E intakes were also related to combined childhood asthma data collected at 1, 2, 5, 10, and 15 years of age. Symptom data were available for 747 (39%) 15-year olds and healthcare data for 1689 (88%). There were no associations between maternal vitamin D and E intakes and childhood wheeze and asthma at age 15. Analysis of combined data collected between 1 and 15 years of age demonstrated that higher maternal vitamin D and E intakes during pregnancy were associated with a reduced likelihood of being diagnosed with asthma in the first 15 years: hazard ratio (95%CI) per quartile increase in vitamin intake of 0.87 (0.78,0.98) and 0.88 (0.78,0.98), respectively. Lower maternal vitamin D and E intakes during pregnancy are associated with increased risk of children wheezing and being diagnosed with asthma in the first 10 years but not after puberty, suggesting that post-natal exposures predominate in the etiology of incident asthma as children transition through puberty into adulthood.

Exposure to air pollution and cognitive functioning across the life course--A systematic literature review.

OBJECTIVES: Air pollution is associated with increased risk of respiratory, cardiovascular and cerebrovascular disease, but its association with cognitive functioning and impairment is unclear. The aim of this systematic review was to examine whether a relationship exists between these variables across the life course. METHODS: We searched Web of Knowledge, Pubmed, SciVerse Scopus, CINAHL, PsychInfo and Science Direct up to October 2015 to identify studies that investigated the association between air pollution and performance on neurocognitive tests. RESULTS: Variations in exposure assessment and outcome measures make meta-analysis impossible. Thirty one studies published between 2006 and 2015, from the Americas (n=15), Asia (n=5) and Europe (n=11), met the criteria for inclusion. Many showed weak but quantified relationships between various air pollutants and cognitive function. Pollution exposure in utero has been associated with increased risk of neuro-developmental delay. Exposure in childhood has been inversely associated with neuro-developmental outcomes in younger children and with academic achievement and neurocognitive performance in older children. In older adults, air pollution has been associated with accelerated cognitive decline. CONCLUSIONS: The evidence to date is coherent in that exposure to a range of largely traffic-related pollutants has been associated with quantifiable impairment of brain development in the young and cognitive decline in the elderly. There is insufficient evidence at present to comment on consistency, in view of the different indices of pollution and end-points measured, the limited number of studies, and the probability at this stage of publication bias. However, plausible toxicological mechanisms have been demonstrated and the evidence as a whole suggests that vehicular pollution, at least, contributes to cognitive impairment, adding to pressure on governments and individuals to continue to reduce air pollution.

Farewell, king coal!

Coal mining provided the power for the industrial development of the West, at great cost to the health of the workforce and, from industrial pollution, of the population. Medical appreciation of the diseases of miners was slow to develop and has been marked by controversy relating to the roles of coal and quartz and the causation of emphysema. Research by the MRC and the British coal industry resolved these issues as the industry itself declined. However, from the research has come an understanding of the influence of inhalation of different inhaled pollutants on human health that has been applied to predicting and preventing possible hazards of developing nanotechnologies.