Hilary Cowie
University of Illinois at Chicago
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BMJ Open | 2012
George Osei-Assibey; Smita Dick; Jennie I. Macdiarmid; Sean Semple; John J. Reilly; Anne Ellaway; Hilary Cowie; Geraldine McNeill
Background and objective The increasing prevalence of childhood obesity has led to interest in its prevention, particularly through school-based and family-based interventions in the early years. Most evidence reviews, to date, have focused on individual behaviour change rather than the ‘obesogenic environment’. Objective This paper reviews the evidence on the influence of the food environment on overweight and obesity in children up to 8 years. Data sources Electronic databases (including MEDLINE, EMBASE, Cochrane Controlled Trials Register (CCTR), DARE, CINAHL and Psycho-Info) and reference lists of original studies and reviews were searched for all papers published up to 31 August 2011. Study selection Study designs included were either population-based intervention studies or a longitudinal study. Studies were included if the majority of the children studied were under 9 years, if they related to diet and if they focused on prevention rather than treatment in clinical settings. Data extraction Data included in the tables were characteristics of participants, aim, and key outcome results. Quality assessment of the selected studies was carried out to identify potential bias and an evidence ranking exercise carried out to prioritise areas for future public health interventions. Data synthesis Thirty-five studies (twenty-five intervention studies and ten longitudinal studies) were selected for the review. There was moderately strong evidence to support interventions on food promotion, large portion sizes and sugar-sweetened soft drinks. Conclusions Reducing food promotion to young children, increasing the availability of smaller portions and providing alternatives to sugar-sweetened soft drinks should be considered in obesity prevention programmes aimed at younger children. These environment-level interventions would support individual and family-level behaviour change.
BMJ Open | 2014
Smita Dick; Amanda J Friend; K Dynes; F AlKandari; Emma Doust; Hilary Cowie; Jon Ayres; Steve Turner
Objectives Childhood asthma is a complex condition where many environmental factors are implicated in causation. The aim of this study was to complete a systematic review of the literature describing associations between environmental exposures and the development of asthma in young children. Setting A systematic review of the literature up to November 2013 was conducted using key words agreed by the research team. Abstracts were screened and potentially eligible papers reviewed. Papers describing associations between exposures and exacerbation of pre-existing asthma were not included. Papers were placed into the following predefined categories: secondhand smoke (SHS), inhaled chemicals, damp housing/mould, inhaled allergens, air pollution, domestic combustion, dietary exposures, respiratory virus infection and medications. Participants Children aged up to 9 years. Primary outcomes Diagnosed asthma and wheeze. Results 14 691 abstracts were identified, 207 papers reviewed and 135 included in the present review of which 15 were systematic reviews, 6 were meta-analyses and 14 were intervention studies. There was consistent evidence linking exposures to SHS, inhaled chemicals, mould, ambient air pollutants, some deficiencies in maternal diet and respiratory viruses to an increased risk for asthma (OR typically increased by 1.5–2.0). There was less consistent evidence linking exposures to pets, breast feeding and infant dietary exposures to asthma risk, and although there were consistent associations between exposures to antibiotics and paracetamol in early life, these associations might reflect reverse causation. There was good evidence that exposures to house dust mites (in isolation) was not associated with asthma risk. Evidence from observational and intervention studies suggest that interactions between exposures were important to asthma causation, where the effect size was typically 1.5–3.0. Conclusions There are many publications reporting associations between environmental exposures and modest changes in risk for asthma in young children, and this review highlights the complex interactions between exposures that further increase risk.
Thorax | 1988
Ken Donaldson; R E Bolton; A. D. Jones; Geraldine M. Brown; M D Robertson; Joan Slight; Hilary Cowie; J. M. G. Davis
The kinetics of the bronchoalveolar response was assessed in rats exposed, at equal airborne mass concentration (10 mg/m3), to titanium dioxide--a non-pathogenic dust--and the two pathogenic mineral dusts quartz and chrysotile asbestos. Rats were killed at intervals over a 75 day exposure period and groups of rats exposed for 32 and 75 days after recovery for two months. Bronchoalveolar lavage was carried out and the lavage fluid characterised for cellular content, macrophage activation, and concentrations of free total protein, lactate dehydrogenase, and N-acetyl-beta-D-glucosaminidase. Inhalation exposure to the two pathogenic dusts resulted in an increased number of leucocytes, macrophage activation, and increased levels of free enzymes and total protein. The pattern and magnitude of the responses to quartz and chrysotile differed. Chrysotile caused less inflammation than quartz, and the main cellular response peaked around the middle of the period of dust exposure whereas the highest levels of enzymes occurred towards the end. The difference in timing suggests that macrophages were not available for lavage towards the end of the exposure, owing to their playing a part possibly in deposition of granulation tissue. Quartz caused a greater cellular and enzyme response than chrysotile, particularly towards the end of the dust exposure phase. There was a noticeable progression of inflammation in the quartz exposed groups left to recover for two months, but not in the chrysotile recovery groups.
Toxicology in Vitro | 2015
Matthew Boyles; Lesley Young; David M. Brown; Laura MacCalman; Hilary Cowie; Anna Moisala; Fiona Ruth Smail; Paula J.W. Smith; Lorna Proudfoot; Alan H. Windle; Vicki Stone
The potential toxicity of carbon nanotubes (CNTs) has been compared to pathogenic fibres such as asbestos. It is important to test this hypothesis to ascertain safe methods for CNT production, handling and disposal. In this study aspects reported to contribute to CNT toxicity were assessed: length, aspect ratio, iron content and crystallinity; with responses compared to industrially produced MWCNTs and toxicologically relevant materials such as asbestos. The impacts of these particles on a range of macrophage models in vitro were assessed due to the key role of macrophages in particle clearance and particle/fibre-induced disease. Industrially produced and long MWCNTs were cytotoxic to cells, and were potent in inducing pro-inflammatory and pro-fibrotic immune responses. Short CNTs did not induce any cytotoxicity. Frustrated phagocytosis was most evident in response to long CNTs, as was respiratory burst and reduction in phagocytic ability. Short CNTs, metal content and crystallinity had less or no influence on these endpoints, suggesting that many responses were fibre-length dependent. This study demonstrates that CNTs are potentially pathogenic, as they were routinely found to induce detrimental responses in macrophages greater than those induced by asbestos at the same mass-based dose.
Thorax | 2011
Jon Ayres; Richard Boyd; Hilary Cowie; J Fintan Hurley
Objectives To estimate the social costs of occupational asthma in the UK. Methods A desk-top approach using cost-of-illness methodology was employed, defining direct and indirect lifetime costs for six scenarios: a male and a female worker each exposed to isocyanates, latex and biocides (eg, glutaraldehyde) or flour. The numbers of new cases annually in each industry were estimated from Survey of Work-related and Occupational Respiratory Disease (SWORD) data. The main outcome measure was the current value total working lifetime costs of new cases annually for each scenario. Results Assuming 209 new cases of occupational asthma in the six scenarios in the year 2003, the present value total lifetime costs were estimated to be £25.3–27.3 million (2004 prices). Grossing up for all estimated cases of occupational asthma in the UK in 2003, this came to £70–100 million. About 49% of these costs were borne by the individual, 48% by the state and 3% by the employer. Conclusions The cost to society of occupational asthma in the UK is high. Given that the number of newly diagnosed cases is likely to be underestimated by at least one-third, these costs may be as large as £95–135 million. Each year a new stream of lifetime costs will be added as a newly diagnosed cohort is identified. Approaches to reduce the burden of occupational asthma have a strong economic justification. However, the economic burden falls on the state and the individual, not on the employer. The incentive for employers to act is thus weak.
Indoor Air | 2012
Sean Semple; Carole Garden; Marie A. Coggins; Karen S. Galea; Paul Whelan; Hilary Cowie; Araceli Sánchez-Jiménez; Peter S. Thorne; J. F. Hurley; Jon Ayres
UNLABELLED There are limited data describing pollutant levels inside homes that burn solid fuel within developed country settings with most studies describing test conditions or the effect of interventions. This study recruited homes in Ireland and Scotland where open combustion processes take place. Open combustion was classified as coal, peat, or wood fuel burning, use of a gas cooker or stove, or where there is at least one resident smoker. Twenty-four-hour data on airborne concentrations of particulate matter<2.5 μm in size (PM2.5), carbon monoxide (CO), endotoxin in inhalable dust and carbon dioxide (CO2), together with 2-3 week averaged concentrations of nitrogen dioxide (NO2) were collected in 100 houses during the winter and spring of 2009-2010. The geometric mean of the 24-h time-weighted-average (TWA) PM2.5 concentration was highest in homes with resident smokers (99 μg/m3--much higher than the WHO 24-h guidance value of 25 μg/m3). Lower geometric mean 24-h TWA levels were found in homes that burned coal (7 μg/m3) or wood (6 μg/m3) and in homes with gas cookers (7 μg/m3). In peat-burning homes, the average 24-h PM2.5 level recorded was 11 μg/m3. Airborne endotoxin, CO, CO2, and NO2 concentrations were generally within indoor air quality guidance levels. PRACTICAL IMPLICATIONS Little is known about indoor air quality (IAQ) in homes that burn solid or fossil-derived fuels in economically developed countries. Recent legislative changes have moved to improve IAQ at work and in enclosed public places, but there remains a real need to begin the process of quantifying the health burden that arises from indoor air pollution within domestic environments. This study demonstrates that homes in Scotland and Ireland that burn solid fuels or gas for heating and cooking have concentrations of air pollutants generally within guideline levels. Homes where combustion of cigarettes takes place have much poorer air quality.
Occupational and Environmental Medicine | 2001
Hilary Cowie; Pascal Wild; J Beck; Guy Auburtin; C Piekarski; N Massin; J W Cherrie; J F Hurley; Brian Miller; S Groat; C A Soutar
OBJECTIVES To investigate possible relations between respiratory health and past airborne exposure to refractory ceramic fibres (RCFs) and respirable dust in workers at six European factories, studied previously in 1987. METHODS The target population comprised all current workers associated with RCF production, plus others who had participated in 1987 “leavers”. Information was collected on personal characteristics, chest radiographs, lung function, respiratory symptoms, smoking, and full occupational history. Regression analysis was used to study relations between indices of health of individual workers and of cumulative exposure to airborne dust and fibres, and likely past exposure to asbestos. RESULTS AND DISCUSSION 774 workers participated (90% of current workers, 37% of leavers). Profusion of small opacities in exposed workers (51% 0/1+; 8% 1/0+) was similar to that among an unexposed control group but higher than in new readings of the 1987 study films (11% 0/1+, 2% 1/0+). The large difference between 1987 and recent films may be, at least in part, a reading artefact associated with film appearance. Small opacities of International Labour Organisation (ILO) category 1/0+ were not associated with exposure. An association of borderline significance overall between 0/1+ opacities and exposure to respirable fibres was found for some exposure periods only, the time related pattern being biologically implausible. Pleural changes were related to age and exposure to asbestos, and findings were consistent with an effect of time since first exposure to RCFs. Among men, forced expired volume in 1 second (FEV1) and forced vital capacity (FVC) were inversely related to exposure to fibres, in current smokers only. FEV1/ FVC ratio and transfer factor (TLCO) were not related to exposures. The estimated restrictive effect was on average mild. Prevalence of respiratory symptoms was low. Chronic bronchitis and its associated symptoms (cough, phlegm) showed some association with recent exposure to respirable fibres. This could be due to an irritant effect of RCFs.
Occupational and Environmental Medicine | 2004
C A Soutar; J F Hurley; Brian Miller; Hilary Cowie; D Buchanan
To help inform the setting of dust control standards in coalmines, this brief review summarises the most recent and reliable exposure-response relations, for damaging respiratory effects, derived from the Pneumoconiosis Field Research (PFR). Collecting data over 38 years in the British coal industry, this was a programme of prospective research on the respiratory health of coal miners, characterised by regular health surveys and detailed measurements of dust and silica concentrations in the workplace. Exposure-response relations are presented for coal workers’ simple pneumoconiosis category II, progressive massive fibrosis, defined deficits of lung function (FEV1), and category II silicosis. This simplified overview provides a guide to the most recent and most reliable estimates from the PFR of dust-related risks of substantial pulmonary disease, and to the magnitude of the effects. Control of dust sufficient to prevent category II simple pneumoconiosis should prevent most cases of progressive massive fibrosis and most dust related large lung function deficits. Where the dust contains high proportions of silica, control to low levels is essential, and even quite brief excursions of silica to high levels must be avoided.
BMJ Open | 2014
Smita Dick; Emma Doust; Hilary Cowie; Jon Ayres; Steve Turner
Objective To complete a systematic review of the literature describing associations between all environmental exposures and asthma symptoms and exacerbations in children up to mean age of 9 years. Design Systematic review. Setting Reference lists of identified studies and reviews were searched for all articles published until November 2013 in electronic databases (MEDLINE, EMBASE, CINAHL, Cochrane Controls Trials Register). Participants Studies were selected which examined a link between exposure to environmental factors and asthma symptoms and exacerbations where the study participants were children with a mean age of ⩽9 years. Primary and secondary outcome measures Indices of asthma symptoms, control and exacerbations. Results A total of 27 studies were identified including eight where inhaled allergens and four where environmental tobacco smoke (ETS) were the exposures of interest. There was evidence that exposure to allergen, ETS, poor air quality and unflued heaters had a modest magnitude of effect (ORs between 2 and 3). There was also evidence of interactions observed between exposures such as allergen and ETS. Conclusions Exposure to inhaled allergens, ETS, unflued heaters and poor air quality has an important effect on exacerbations in young children with asthma and should be minimised or, ideally, avoided. Better understanding of the effect of exposure to damp housing, air conditioning and dietary factors plus interactions between environmental exposures associated with exacerbations is required.
Occupational and Environmental Medicine | 1997
R G Love; Brian Miller; S K Groat; S Hagen; Hilary Cowie; P P Johnston; P A Hutchison; C A Soutar
OBJECTIVE: To identify whether there is evidence of pneumoconiosis and other respiratory health effects associated with exposure to respirable mixed dust and quartz in United Kingdom opencast coalmines. METHODS: A cross sectional study of current workers (1224 men, 25 women) was carried out at nine large and medium sized opencast sites in England, Scotland, and Wales. To characterise a range of occupational groups within the industry, full shift measurements of personal exposures to respirable dust and quartz were taken. Up to three surveys were carried out at each site, covering all four seasons. For the purposes of comparisons with health indices these groups were further condensed into five broad combined occupational groups. Full sized chest radiographs, respiratory symptoms, occupational history questionnaires, and simple spirometry were used to characterise the respiratory health of the workforce. Logistic or multiple regression techniques were used to examine relations between indices of exposure and respiratory health. RESULTS: None of the group geometric mean dust concentrations, based on 626 valid dust samples, exceeded 1 mg.m-3, and 99% of all quartz concentrations were below 0.4 mg.m-3, the current maximum exposure limit. The highest quartz concentrations were experienced by the rock drilling team and drivers of bulldozers (used to move earth and stone from layers of coal). There were clear differences in mean respirable dust and quartz concentrations between occupational groups. These were consistent across the different sites, but depended in part on the day of measurement. The variations between sites were not much greater than between days, suggesting that differences between sites were at least partly explained by differences in conditions at the time of the measurements. The prevalence of radiographic small opacities profusion category > or = 1/0, based on the median of three readings, was 4.4%. Five men had category 2 pneumoconiosis and two men (including one of these five) had progressive massive fibrosis category A. From regression analyses, the relative risk of attaining a profusion of category > or = 0/1 was estimated to be doubled for every 10 years worked in the dustiest, preproduction opencast jobs, after allowing for age, smoking, and site effects. Risk was not associated with time worked in any other occupation within the industry, nor with previous employment in underground mining or other dusty jobs. Symptoms of chronic bronchitis were present in 13% of the men. Frequency of chronic bronchitis was influenced by years worked in dusty jobs outside opencast mining, but not by time spent in occupations within the industry. Asthmatic symptoms were reported by 5% of the workforce, close to the mean frequency found in adult men. No positive associations were found between asthma and occupational exposures. Lung function on average was close to predicted value and showed no relation to time worked in opencast occupations. CONCLUSIONS: Frequency of (mostly mild) chest radiographic abnormalities is associated with working in the dustier, preproduction jobs in the industry. Although some of these mild abnormalities may be non-occupational (due to aging or smoking), the association with exposure indicates a small risk of pneumoconiosis in these men, and the need to monitor and control exposures, particularly in the high risk occupations.