Displaying 1-10 letters out of 243 published
Re:Extreme temperatures and paediatric emergency
Dear Sir, Thank you very much for your interest in our research. In our JECH paper, we analyzed data on a broad range of pediatric diseases and found, generally, children aged 10-14 years are more vulnerable to both hot and cold effects, compared with children of other age groups. In the OEM paper, we analyzed pediatric asthma data and found, specifically, children aged 10-14 years are more sensitive to the adverse impact of cold on asthma. We used consistent statistical approach in the two papers and have controlled for relative humidity and air pollutants. Due to limited space, we were not be able to present the difference between different age groups in terms of vulnerability to temperature effects on every disease. Best, Zhiwei
Conflict of Interest:
Trajectories for each cohort need to span the same/ similar age range
The three cohorts in this study were as follows:
Cohort 1: born 1970s and followed between ~15-35 years of age
Cohort 2: born 1950s and followed between ~35-55 years of age
Cohort 3: born 1930s and followed between ~55-75 years of age
This study design has serious limitations for the investigation of cohort differences in BMI trajectories (and therefore also for the investigation of cohort differences in the associations of socio-economic position with BMI trajectory). Looking at Figure 1 - how, for example, can you calculate cohort differences in BMI at age 45 years when only cohort 2 had data at that age? How, in fact, can you make any cohort comparison of trajectories at ages when only one cohort had data? The mixed effects model used in the present paper will provide estimates, but these are based on trajectories fitted beyond the age range of the data (for at least one cohort). The only ages were cohort differences could have reliably been estimated are those were there is overlap (e.g., difference in BMI at age 35 years between cohort 1 and cohort 2), and this could have been done with cross-sectional analyses.
Failure to consider the limitations of the data has led to potentially misleading interpretation of the results, such as "adiposity increased most quickly with age in the youngest cohort". This is expected given that cohort 1 was of an age where BMI is known to increase more rapidly than later in life. The design of the study makes it impossible to disentangle age and cohort effects (except at overlapping ages). For example, is BMI at baseline greater in cohort 3 than in cohort 1 because they are different cohorts (exposed to different environments) or because they are different ages? The difference will, of course, be due to a combination of age and cohort effects, plus any possible period effect.
Cross-cohort comparisons of trajectories are a powerful strategy, but in nearly all instances they require the trajectories for each cohort to span the same or similar age range.
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Is 7 a day really better than 5 a day?
These impressive data have been widely reported. Eating plenty of fruit and vegetables seems to be a good idea, but I am concerned at how the need to eat 7+ portions a day to obtain maximum benefit has been reported. As far as I can tell, the estimates for "daily" consumption were based on a single day. Few people eat exactly the same every day and regression to the mean suggests that most of those who ate 7+ portions on the day of the survey will not have sustained such high levels of consumption over the 7.7 years of follow-up. While these people probably continued to eat a lot of fruit and vegetables and gain health benefits from doing so, isn't it misleading to extrapolate the quantity of fruit and vegetable eaten in one day into a recommendation for regular daily consumption?
Conflict of Interest:
Re:What exactly is a vegetable?
Dear Prof. Bland,
Please see our supplementary material where you can see the questions that were asked during the interview. You will note that survey participants were explicitly advised not to include potatoes when considering their answers.
Conflict of Interest:
Air pollution and respiratory symptoms in children
Molter et al. reported the effects of long-term exposure to particulate matter with aerodynamic diameter <10 micrometer (PM10) and nitrogen dioxide (NO2) on the prevalence of asthma and wheeze within a population-based birth cohort (1). They concluded that no significant association between long-term exposure to PM10 and NO2 and the prevalence of either asthma or wheeze was found. In contrast, the same authors reported that lifetime exposure to PM10 and NO2 was associated significantly with reductions in lung volume growth by using the same cohort (2).
On this point, Gehring et al. conducted meta-analysis with random- effect model on the effects of air pollution on lung function in children (3). They concluded that that current levels of NO2, total nitrogen oxides, and particulate matter with aerodynamic diameter <2.5 micrometer (PM2.5) were significantly associated with the change in forced expiratory volume in 1 second (FEV1), but PM10 showed no significance. As the level of statistical significance in studies by Molter et al. or Gehring et al. was not highly enough, final conclusion cannot be determined. Relating to these studies, Urman et al. reported health survey to assess the effects of near-roadway air pollution (NRAP) and regional pollution on childhood lung function (4). They concluded that the contribution of regional pollution to adverse lung function, evaluated by FEV1 and forced vital capacity (FVC), was relatively larger than that of NRAP, and NO2 contributed little to the decrease in FEV1 and FVC than other air pollution indicators such as PM2.5 and PM10.
I have some concerns on the study outcomes. First, physiological lung functions and subjective respiratory complains for dependent variables would sometimes lead to the different study outcome, and both dependent factors should be evaluated to know the adverse effect of air pollution on respiratory organs. As one of the co-authors, I conducted questionnaire survey for 16,663 pairs of junior high school students and their mothers in Indonesian cities to measure the effect of air pollution on respiratory health (5). Nine communities were set and there were inter-class and intra -class variation of NO2. As a main result, the prevalence rates of the symptoms of cough, phlegm, persistent cough, wheezing without a cold, and asthma of the student were significantly correlated with the NO2 emitted along large roads near their residences.
Second, the superiority of PM2.5 compared with PM10 could not be confirmed, and the best aerodynamic diameter of particulate matter as an air pollution indicator should be specified by further studies.
Finally, I recommend for considering indoor air pollution especially by smoking (6). Anyway, cause-effect relationship would be clarified by epidemiological cohort studies.
1 Molter A, Agius R, de Vocht F, et al. Effects of long-term exposure to PM10 and NO2 on asthma and wheeze in a prospective birth cohort. J Epidemiol Community Health 2014;68:21-8.
2 Molter A, Agius RM, de Vocht F, et al. Long-term exposure to PM10 and NO2 in association with lung volume and airway resistance in the MAAS birth cohort. Environ Health Perspect 2013;121:1232-8.
3 Gehring U, Gruzieva O, Agius RM, et al. Air Pollution Exposure and Lung Function in Children: The ESCAPE Project. Environ Health Perspect 2013;121:1357-64.
4 Urman R, McConnell R, Islam T, et al. Associations of children's lung function with ambient air pollution: joint effects of regional and near-roadway pollutants. Thorax 2013 Nov 19. doi: 10.1136/thoraxjnl-2012- 203159.
5 Duki MI, Sudarmadi S, Suzuki S, et al. Effect of air pollution on respiratory health in Indonesia and its economic cost. Arch Environ Health 2003;58:135-43.
6 Guerra S, Stern DA, Zhou M, et al. Combined effects of parental and active smoking on early lung function deficits: a prospective study from birth to age 26 years. Thorax 2013;68:1021-8.
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What exactly is a vegetable?
I may have missed it, but Oyebode et al. do not seem to say exactly what they mean by a vegetable or what the exact question was. This is important, because they do refer to a UK Department of Health website, which states that potatoes, yams, plantain, and casava should not be included the 5-a-day count, but sweetcorn should. I thought that sweetcorn was a grain and so would not count it as a vegetable, though I may be wrong, but if asked how many portions of vegetables I ate yesterday would definitely have included potatoes, a staple food in the UK, if I had eaten them. I think that the authors should clarify this.
Conflict of Interest:
Extreme temperatures and paediatric emergency
Sir, the recent report on "extreme temperatures and paediatric emergency" is very interesting . Xu et al. concluded that "children are at particular risk of a variety of diseases which might be triggered by extremely high temperatures ."Xu et al. also mentioned for the effect of climate change. In fact, Xu et al. reported a highly similar publication in Occup Environ Med and also noted for the effect of climate change on childhood illness with special focus on asthma . The two works should share the same groups of patients but the conclusion is different. In the present report, Xu et al. make a conclusion that "children aged 10-14 years were more sensitive to both hot and cold effects " whereas they proposed that "children aged 10-14 years were most vulnerable to cold effects ." This implies that there are many bias in both reports. Hence, it cannot conclude on any effects from hot and cold temperature on pediatric illness. In addition, not only temperature but also other climatic factors can affect the disease incidence. The good example is the effect of humidity , pollutants  and ozone levels .
1. Xu Z, Hu W, Su H, Turner LR, Ye X, Wang J, Tong S. Extreme temperatures and paediatric emergency department admissions. J Epidemiol Community Health. 2013 Nov 23. doi: 10.1136/jech-2013-202725. [Epub ahead of print] 2. Xu Z, Huang C, Hu W, Turner LR, Su H, Tong S. Extreme temperatures and emergency department admissions for childhood asthma in Brisbane, Australia. Occup Environ Med. 2013 Oct;70(10):730-5. 3. Vandini S, Corvaglia L, Alessandroni R, Aquilano G, Marsico C, Spinelli M, Lanari M, Faldella G. Respiratory syncytial virus infection in infants and correlation with meteorological factors and air pollutants. Ital J Pediatr. 2013 Jan 11;39(1):1. 4. Jones GN, Sletten C, Mandry C, Brantley PJ. Ozone level effect on respiratory illness: an investigation of emergency department visits. South Med J. 1995 Oct;88(10):1049- 56.
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Re: Social determinants of mental health: a Finnish nationwide follow up study on mental disorders
Dear Editor, The published paper by Paananen et al, entitled "Social determinants of mental health: a Finnish nationwide follow up study on mental disorders"1 was an interesting and rigorous study. Through a longitudinal approach, all Finnish children who were born in a certain year (1987) were followed through adolescence in order to examine the development of mental disorders and assess potential SDH-related risk factors. For this purpose, the authors created six multivariate models between different groups of variables and the outcome. In addition, a full model was developed to include the variables which showed significant associations with the outcome in at least one of these six models. In Table 2 of that paper, the determinants of mental disorders according to various models were demonstrated. Nevertheless, it was not clear for us why parent's highest educational level, parent's highest SES, parental social assistance, cohort member's education and cohort member's received social assistance which showed association with the outcome in models 2, 3 or 5, were not included in the full model. At the first look, one might speculate that these variables were included in the full model, but were not shown in Table 2; as they might not have proved significant. But, this might not be the correct justification as some non-significant variables e.g. "mother's age (<20)" and "single mothers" could be found in the full model within the same table without being significant in the full model. It would be very kind of the authors to respond to this question and explain whether it would be a concern in the main findings of the full model or not. Sincerely Yours, * Narjes Hazar, MD, Resident in Community Medicine, Department of Community Medicine, Tehran University of Medical Sciences, Tehran, Iran * Mojgan Karbakhsh, MD, Associate Professor in Community Medicine, Department of Community Medicine, Tehran University of Medical Sciences, Tehran, Iran Reference: 1. Paananen R, Ristikari T, Merikukka M, Gissler M. Social determinants of mental health: a Finnish nationwide follow-up study on mental disorders. J Epidemiol Community Health. 2013 Aug 1. doi:10.1136/jech-2013-202768 ________________________________________________________________________ Corresponding author: Dr Narjes Hazar, MD, Resident in Community Medicine, Department of Community Medicine, Tehran University of Medical Sciences, Tehran, Iran Address: Department of Community Medicine, School of Medicine, Tehran University of Medical Sciences, PoorSina St, Qods St, Enqelab Av, Tehran, Iran Email: email@example.com Tel/Fax: +9821 88962357
Conflict of Interest:
Cochrane review of health & socio-economic impacts of housing improvement
This is a great contribution to the literature on fuel poverty, cold housing, and health.
The authors call for a review of qualitative and intervention research related to this topic. It may be useful for readers to be made aware of a recently updated version of a systematic review of the health and socio-economic impacts of housing improvement published by the Campbell and Cochrane Collaborations 1. In this review we looked at physical improvements to housing infrastructure and this included a group of 15 quantitative (including five RCTs) and seven qualitative studies of warmth & energy efficiency improvements. We did not include studies which only looked at financial help with fuel bills, for example the winter fuel allowance distributed to the elderly in the UK.
1. Thomson H, Thomas S, Sellstrom E, Petticrew M. Housing improvements for health and associated socio-economic outcomes. Cochrane Database of Systematic Reviews 2013;2:Art. No.: CD008657 DOI: 10.1002/14651858.CD008657.pub2. http://onlinelibrary.wiley.com/doi/10.1002/14651858.CD008657.pub2/pdf/standard
Conflict of Interest:
Flagging up my own work.
TTC places public health at risk
Pesticide Action Network Europe It cannot be denied that TTC (Threshold of Toxicological Concern) was originally proposed in the U.S., as Dr Harris states in her commentary on our article, but her industry-sponsored organisation, the International Life Sciences Institute (ILSI) played a major role in developing it further to the form in which it was accepted by European Food Safety Authority (EFSA). This process took place in an EFSA working group, in which ten out of 13 members had previously developed and promoted the tool with ILSI. While EFSA communicators have attempted damage control in their online Q&A, the biased work on TTC raised such concerns in the European Parliament that EFSA was forced to ban ILSI-linked people from being members of expert panels and working groups. Any link with ILSI now has to be cut in order to qualify as an EFSA expert. Apart from this industry infiltration of EFSA, the tool as delivered by ILSI is far from being "scientifically supported", as Dr Harris suggests. The database underpinning the TTC for non-genotoxic substances is entirely made up of (potentially biased) industry studies. Many of these studies are 40-60 years old and non-retrievable (cannot be accessed), meaning that their quality cannot be assessed. In addition, the old protocols used means that current scientific knowledge will not be taken into account in calculating TTCs. In utero exposure is generally missing and important risks will be overlooked because of the limited endpoints considered at that time. The grouping of chemicals for TTC is artificial and is based on the Cramer classification, which relies on expert judgement only and is subjective. ILSI has also manipulated the genotoxin database to get to an apparently desired outcome. For example, it has removed aflatoxin-like, azo- and N-nitroso- substances. Another unscientific shortcoming of TTC is its disregard of cumulative effects. The TTC is derived by arbitrarily removing from the calculation the most toxic effects found in the database of NOELs (no adverse effect levels). The TTC sets the 'level of no concern' at the 5th percentile, resulting in a 1 in 20 chance that a random substance in any one group of chemicals is toxic at this exposure level. Thus 5% of the chemicals in the group are more toxic than the 'level of no concern' that is set for any one group of chemicals. TTC is promoted as a screening tool while in practice it is already being used as a cut-off criterion (safe level) for pesticide metabolites. Industry is now trying to extend TTC to other fields such as any chemical found in food, outcomes of developmental testing, drinking water, and inhaled chemicals. In many cases, and not coincidentally, advocates of TTC are pursuing these aims through opinions published in Regulatory Toxicology and Pharmacology, the controversial chemical/pharmaceutical industry-sponsored journal. The journal was one of several entities that were investigated by a US Congressional Committee in 2008 over their role in the Food and Drug Administration (FDA) decision allowing bisphenol A in infant formula and other foods.[11-13] Analysing the TTC tool and the background of its development can only lead to the conclusion that industry has invested massively in a tool that does not safeguard human health, as Dr Harris misleadingly claims, but exactly the opposite. The tool serves industry's agenda of fast-tracking chemicals to the market and avoids the costs of testing. The tool undermines European legislation and policy. It aims to replace the existing EU policy of 'no safe level' for genotoxic substances with claimed 'safe levels' arrived at through the TTC. It also aims to replace the EU policy that health of citizens should be protected by adequate testing and the precautionary principle with a tool that enables avoidance of testing for chemicals, metabolites and impurities. The tool, which serves industry's agenda but places public health at risk, has been introduced into European agencies by people who have served as members of expert panels while maintaining conflicts of interest with industry. Dr Harris's reference to the Danish study as a balanced review of TTC is a case in point. Its author, John Christian Larsen, worked in ILSI scientific bodies from 2002 till 2008 and has published studies with ILSI-affiliated people who have promoted TTC. TTC has made its way into the regulatory policy of the food safety authority EFSA because of industry's massive resources and a lack of awareness on the part of EFSA's staff, not for reasons of sound science.
1. Robinson C, Holland N, Leloup D, et al. Conflicts of interest at the European Food Safety Authority erode public confidence. J Epidemiol Community Health Published Online First: 8 March 2013. doi:10.1136/jech- 2012-202185
2. Muilerman H, Tweedale T. A toxic mixture? Industry bias found in EFSA working group on risk assessment for toxic chemicals, Pesticide Action Network Europe 2011.
3. EFSA Scientific Committee. Scientific opinion on exploring options for providing advice about possible human health risks based on the concept of Threshold of Toxicological Concern (TTC). EFSA Journal 2012;10: 2750.
4. Cramer GM, Ford RA, Hall RL. Estimation of toxic hazard - a decision tree approach. Food Cosmet Toxicol 1978;16: 255-276.
5. Kroes R, Renwick AG, Cheeseman M, et al. Structure-based thresholds of toxicological concern (TTC): guidance for application to substances present at low levels in the diet. Food Chem Toxicol 2004; 42: 65-83.
6. European Commission Health and Consumer Protection Directorate- General (DG SANCO). Guidance document on the assessment of the relevance of metabolites in groundwater of substances regulated under Council Directive 91/414/EEC: Sanco/221/2000-rev.10-final. 25 February 2003.
7. Koster S, Boobis AR, Cubberley R, et al. Application of the TTC concept to unknown substances found in analysis of foods, Food and Chemical Toxicology 2011; 49: 1643-1660.
8. Van Ravenzwaay B, Dammann M, Buesen R, et al. The threshold of toxicological concern for prenatal developmental toxicity. Regulatory Toxicology and Pharmacology 2011;59: 81-90.
9. Melching-Kollmuss S, Dekant W, Kalberlah F. Application of the ''threshold of toxicological concern" to derive tolerable concentrations of ''non-relevant metabolites" formed from plant protection products in ground and drinking water. Regulatory Toxicology and Pharmacology 2010; 56: 126-134.
10. Escher SE, Tluczkiewicz I, Batke M, et al. Evaluation of inhalation TTC values with the database RepDose. Regulatory Toxicology and Pharmacology 2010; 58: 259-274.
11. Michaels, D. Doubt Is Their Product: How Industry's Assault on Science Threatens Your Health. Oxford University Press. 2008: 53-54.
12. Layton L. Studies on chemical in plastics questioned. Washington Post 27 April 2008.
13. Dingell JD. Letter to Jack N Gerard, president and CEO, American Chemistry Council. 2 April 2008. http://bit.ly/ZWMbi6 (accessed 15 April 2013).
14. Nielsen E, Larsen JC. The Threshold of Toxicological Concern (TTC) concept: Development and regulatory applications. Danish Ministry of the Environment, Environmental Protection Agency. Environmental Project No. 1359. 2011. http://www2.mst.dk/udgiv/publications/2011/03/978-87-92708 -86-1.pdf (accessed 15 April 2013).
15. European Food Safety Authority (EFSA). Declarations of interests (DoIs). http://www.efsa.europa.eu/en/efsawho/doi.htm (accessed 15 April 2013).
16. Pratt I, Barlow S, Kleiner J, et al. The influence of thresholds on the risk assessment of carcinogens in food. Mutation Research 2009; 678: 113-117.
Conflict of Interest:
Hans Muilerman is employed at Pesticide Action Network Europe, which receives funding from trusts and foundations, including the European Endocrine Health Initiative.
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