The minefield of diesel emissions

The carcinogenic effects of diesel emissions/exhaust are widely known. In 1988, the US’ National Institute for Occupational Safety and Health labelled diesel exhaust as a potential occupational carcinogen and, in June 2012, the IARC will be revisiting their existing labelling of diesel particulates as potential carcinogens.

Particulate Matter (PM) in diesel emission
The problematic component of diesel emissions is particulate matter, a topic which yours truly has worked on rather extensively; also, many are the research papers on the morbidity and mortality of PM. PM is an aggregated mixture of salts, inorganic, and organic compounds, generally characterised by aerodynamic diameter. The PM in diesel emissions are collectively very fine (less than 1 μm in diameter) and carbonaceous; but its specific composition depends on the engine characteristics, type of fuel used, and any filtering devices utilised.

Effect of PM on human health
Nonetheless, the end result is that due to their small size, they can penetrate deeply and cause inflammation. Scientists have analysed PM’s distribution in the human lung and sites with PM deposition were predicted to be future sites of lung cancers. On the whole, short-term effects are usually respiratory related. Long-term effects includes respiratory illnesses (ranging from pulmonary inflammation to allergies), cancer, cardiovascular, and cardiopulmonary disease (for more information/references on all statements: contact me)- and even altering of gene expression. But many are the studies associating traffic with increased incidences of respiratory and cardiovascular problems.

Furthermore, the particle’s surface adsorbs polycyclic aromatic compounds, often with metals and acidic components (some examples being chlorobenzene, quinines, acids, benzo-a-pyrene, mercury, lead, phenols). In fact, is there a need to refer to published research when our old elementary chemistry lessons should suffice in deducing what happens if those compounds enter into our body via our nostrils? (for more information/references: contact me).

Diesel exhaust and miners
In this backdrop, consider the situation of those working in underground mines. Miners are the occupational group most exposed to high levels of diesel since they use diesel-powered heavy equipment and breathe in the exhaust on a daily basis. Despite the presence of ventilation (if any), in such an enclosed environment, the exhausts culminates in a very high level. Consequently, researchers at the National Cancer Institute (NCI) and the National Institute for Occupational Safety and Health, via their ‘Diesel Exhaust in Miners Study’, aimed at evaluating the risk of diesel exhaust-associated death in miners, with a sample of 12315 US miners at eight non-metal (to minimise confounding variables such as exposure to carcinogens such as radon, silica, and asbestos) mining facilities (1 limestone mine in Missouri, 3 potash mines in New Mexico, 1 salt mine in Ohio, and 3 trona mines in Wyoming).

Four methodology papers were published in the Annals of Occupational Hygiene in 2010. Subsequently, the results were published in March 2012 via two papers. Paper 1 presented the risk of death from any cause (with an emphasis on lung cancer), using data from the full study population (the cohort study). Paper 2, the case-control study, reported the lung cancer deaths in the cohort study, controlling for smoking and other risk factors (such as prior employment in high-risk jobs, history of respiratory diseases, etc). The dose-response results were illuminating and statistically significant, generally illustrating an increasing risk of lung cancer death with increasing levels of diesel exhaust exposure:

1. Those exposed to high levels of diesel exhaust had three-fold risks of lung cancer (than those exposed to low levels)

2. Those exposed to high levels of diesel exhaust underground faced a five-fold risk.

3. In non-smokers, the risk of lung cancer death increased with increasing exposure to diesel exhaust. Those with the highest level of diesel exposure were 7-times more likely to die from lung cancer than non-smokers in the lowest exposure category.

4. In heavy smokers, the effect of diesel exhaust exposure was attenuated (decreased risk for lung cancer death- decreasing with increasing levels of exposure). It is hypothesised that smoking clears the diesel particulates from the lungs. Furthermore, carcinogens in diesel exhaust and cigarette smoke may operate in the same metabolic pathway in the body and compete with each other, resulting in a saturation of the pathway, thus diminishing the effects of either component (NCI, 2012).

Industry’s ire

Let’s take a detour and visit the mining industry queen bees in their comfy airconditioned offices, far away from the worker bees languishing in an environment of PM-emitting machines. In around 1995, a coalition of mining firms (the Mining Awareness Resource Group) commenced a 17-year legal, legislative, and political battle from conducting and publishing the afore-mentioned epidemiological studies. Their first strategy was to stop the study before it began (after all, is there truly any causal link between diesel exposure and lung cancer incidences?). Their next was to control the release of the study findings using quite a many gimmicks, such as asking for reviewing the data before publication, holding the researchers in contempt of court for withholding data, and writing vaguely threatening letters to journals which may potentially publish the studies.

Potential impacts

The publication of these studies could have the following consequences which affects the industry’s existence and market performance: (rational)investors may withdraw, concerned stakeholders could kick up some troubles, new regulations and standards on diesel emissions, cleaning up, and finding alternatives (all which contributes to compliance costs), and, potentially, miners and their families could sue.

Corporate Human Responsibility, anyone?

What puzzled me was the effort which the coalition put into preventing the studies from being published. In all probabilities, they deduced that the results would not be conducive to their existing status quo. What certainly doesn’t seem to have been considered, by these interested parties (comprising of humans), was the health of their workforce (also comprising of humans). Surely even the rational profit-maximising decision-maker should have deduced that the well-being of the human capital would contribute to long-term firm performance? Politicians too seem to have stood with the industry on this matter. Hypothetically, had the study found no correlation, the studies would probably have been well-publicised by the industry.

External validity

Whilst this study focussed only on the miners, one could extrapolate this to populations/individuals elsewhere exposed to the analysed levels of diesel exhausts. Several countries in the developing world (where emission standards are practically nonexistent) widely use diesel as a vehicle fuel and there is a concentration of usage in trucking, shipping, and rail works. Even if these individuals are not immediately exposed to levels experienced by the underground miners, this could result in a cumulative accumulation. And one needn’t elaborate more on the plight of mine workers in developing countries. One must also point out that lung cancer is just one of the many worries facing a miner.

I hope that the interested parties would view this event as something which could be a source of competitive advantage. For instance, they could develop new technology which further reduces diesel emissions or switch to much more efficient and healthier technologies.

Image source: Gaetano/Corbis

Sources:
Silverman, D., Samanic, C., Lubin, J., Blair, A., Stewart, P., Vermeulen, R., Coble, J., Rothman, N., Schleiff, P., Travis, W., Ziegler, R., Wacholder, S., & Attfield, M. (2012). The Diesel Exhaust in Miners Study: A Nested Case-Control Study of Lung Cancer and Diesel Exhaust JNCI Journal of the National Cancer Institute DOI: 10.1093/jnci/djs034 Attfield, M., Schleiff, P., Lubin, J., Blair, A., Stewart, P., Vermeulen, R., Coble, J., & Silverman, D. (2012). The Diesel Exhaust in Miners Study: A Cohort Mortality Study With Emphasis on Lung Cancer JNCI Journal of the National Cancer Institute DOI: 10.1093/jnci/djs035 Stewart, P., Vermeulen, R., Coble, J., Blair, A., Schleiff, P., Lubin, J., Attfield, M., & Silverman, D. (2012). The Diesel Exhaust in Miners Study: V. Evaluation of the Exposure Assessment Methods Annals of Occupational Hygiene, 56 (4), 389-400 DOI: 10.1093/annhyg/mes020

http://www.cancer.gov/newscenter/pressreleases/2012/DieselMinersQandA http://www.washingtonpost.com/national/health-science/diesel-reports-publication-delayed-as-industry-demands-to-see-documents-first/2012/02/01/gIQA5wrFtQ_story_1.html

Effect of climate change on human morbidity and mortality and sea levels

Climate change has been resulting in quite a many detrimental manifestations which tend to have a domino effect: fluctuations in temperature and precipitation (resulting in climate variability), as well as extreme manifestations such as drought, storms, rise in sea levels, and frequent severe weather events.

Consider the research by Grinsted et al (2009) who used a ‘physically plausible four parameter linear response equation’ to relate nearly 2,000 years of global temperatures and sea level. Assuming that this relationship holds from 200 to 2100 AD, IPCC’s temperature scenarios and reconstructed past sea level scenarios were used to visualise future sea level scenarios. The result suggests that climate change will lead to a 0.9-1.3 m change in sea level between 2090-2099. This bodes a certain flooding of low lying coastal regions and islands. Island countries such as Maldives would practically cease to exist. Whilst countries such as Bangladesh may not face such obliteration, such a sea level rise would flood 1/3rd of the country, displacing millions of humans and severely affecting agriculture, irrigation, and livestock.

Climate change also has a perceptible impact on human morbidity and mortality (Patz et al, 2005). Climate fluctuations have been linked to diseases and ailments- the evident effects of heat/cold (which, for instance, follows a U-shaped dose-response function with increased mortality in the extreme heat and cold), traumatic physical and mental ailments, and even cardiovascular and respiratory illnesses. This even results in altered transmission of infectious diseases (for instance, changes in temperature has been associated with salmonellosis in Europe and cholera in the ‘American south-west’; whilst, changes in rainfall has been associated with Rift valley fever in East Africa, and Hantavirus pulmonary syndrome and cholera in the American south-west and Bangladesh). When one factors in the effects of climate change on air pollution and the greater ecosystem, the result is quite chaotic. If the future projections of climate change are plausible, then it is likely that these health risks may rise significantly. The ‘potentially vulnerable’ regions includes the temperate latitudes (which may warm disproportionately), and the regions in and around the Pacific and Indian oceans (substantial rainfall variability).

But even though the economic North/developed countries are responsible for most of the greenhouse gas emissions, the damaging effects of their actions are most perceived in the poor countries of the South which has (as of yet) contributed least towards the GHG emissions.

References:
Patz, J., Campbell-Lendrum, D., Holloway, T., & Foley, J. (2005). Impact of regional climate change on human health Nature, 438 (7066), 310-317 DOI: 10.1038/nature04188

Grinsted, A., Moore, J., & Jevrejeva, S. (2009). Reconstructing sea level from paleo and projected temperatures 200 to 2100 ad Climate Dynamics, 34 (4), 461-472 DOI: 10.1007/s00382-008-0507-2

Lead: Part 1

Having highlighted a recent paper on the presence of Lead in game, I have decided to commence a series of specialised ‘limelights’ on the effects of Lead bullets/pellets in humans as a result of game hunting. However, before I address my assignment, I shall first provide a succinct background on Lead’s toxicity.

Inception
For thousands of years, Lead has been widely extracted and used by mankind, mainly due to the availability of its many ores as well as its malleability. In fact, Lead used to be the second most used metal (after Iron).

Lead’s toxicity
Despite its many benefits, Lead’s detrimental effects of morbidity and mortality in humans and animals have been demonstrated by numerous studies. These vary from mild manifestations (such as fatigue, emotional irritability, and insomnia) to the fatal conclusion of death. Published studies have established the following:
- reduced somatic growth (Hauser et al, 2008)
- impaired motor function (Cecil et al, 2008)
- decreased brain volume (Cecil et al, 2008)
- permanent cognitive damage, attention and behavioural dysfunction/problems, impaired cognitive function (Needleman et al, 2002; Canfield et al, 2003; Lanphear et al, 2005; Braun et al, 2006; Schnaas et al, 2006; Cecil et al, 2008; Jusko et al, 2008; Wright et al, 2008)
- reproductive damage, including spontaneous abortion (Borja-Aburto et al, 1999)
- nephropathy (Ekong et al, 2006)
- cancer and cardiovascular disease (Lustberg and Silbergeld, 2002; Menke et al, 2006)
- and even criminal behavior (Needleman et al, 2002; Wright et al, 2008).

A great danger of Lead toxicity is that the symptoms may lag physiological changes, i.e. the affected individual may remain unaware of the danger (similar to the effect of cholesterol). Lead in the blood does not excrete and a major proportion sequesters in soft tissues and bone from where it may be switched on especially during pregnancy (Tellez-Rojo et al, 2004) or old age (Schwartz and Stewart, 2007).

Over the past 50 years, as a result of new studies revealing the toxic effects of Lead at lower levels, the benchmark levels have declined (60 μg/dL in 1960; 25 μg/dL in 1985; and, 10 μg/dL in 1991) (Needleman, 2004). And although the current CDC benchmark level is 10 μg/dL, the published studies indicate that it would be inane to consider even a trifling level of Lead exposure as being harmless (Bellinger and Bellinger, 2006)- for instance, Lanphear et al (2005) has associated maximal blood Lead levels lower than 7.5 μg/dL with permanent cognitive damage and intellectual deficits in children, whilst Menke et al (2006) associated 2 µg/dL as having increased risk of cardiovascular mortality in adults.

Foetuses, children, and pregnant women face the greatest risk (Schnaas et al, 2006; Iqbal et al, 2009).

References:

Borja-Aburto VH, Hertz-Picciotto I, Rojas Lopez M, Farias P, Rios C, & Blanco J (1999). Blood lead levels measured prospectively and risk of spontaneous abortion. American journal of epidemiology, 150 (6), 590-7 PMID: 10489998

Lustberg, M. (2002). Blood Lead Levels and Mortality Archives of Internal Medicine, 162 (21), 2443-2449 DOI: 10.1001/archinte.162.21.2443

Needleman HL, McFarland C, Ness RB, Fienberg SE, & Tobin MJ (2002). Bone lead levels in adjudicated delinquents. A case control study. Neurotoxicology and teratology, 24 (6), 711-7 PMID: 12460653

Canfield, R., Henderson, C., Cory-Slechta, D., Cox, C., Jusko, T., & Lanphear, B. (2003). Intellectual Impairment in Children with Blood Lead Concentrations below 10 μg per Deciliter New England Journal of Medicine, 348 (16), 1517-1526 DOI: 10.1056/NEJMoa022848

Needleman, H (2004). Lead poisoning Ann. Rev. Med (55), 209-222

Téllez-Rojo MM, Hernández-Avila M, Lamadrid-Figueroa H, Smith D, Hernández-Cadena L, Mercado A, Aro A, Schwartz J, & Hu H (2004). Impact of bone lead and bone resorption on plasma and whole blood lead levels during pregnancy. American journal of epidemiology, 160 (7), 668-78 PMID: 15383411

Lanphear BP, Hornung R, Khoury J, Yolton K, Baghurst P, Bellinger DC, Canfield RL, Dietrich KN, Bornschein R, Greene T, Rothenberg SJ, Needleman HL, Schnaas L, Wasserman G, Graziano J, & Roberts R (2005). Low-level environmental lead exposure and children's intellectual function: an international pooled analysis. Environmental health perspectives, 113 (7), 894-9 PMID: 16002379

Bellinger DC, & Bellinger AM (2006). Childhood lead poisoning: the torturous path from science to policy. The Journal of clinical investigation, 116 (4), 853-7 PMID: 16585952

Braun JM, Kahn RS, Froehlich T, Auinger P, & Lanphear BP (2006). Exposures to environmental toxicants and attention deficit hyperactivity disorder in U.S. children. Environmental health perspectives, 114 (12), 1904-9 PMID: 17185283

Ekong EB, Jaar BG, & Weaver VM (2006). Lead-related nephrotoxicity: a review of the epidemiologic evidence. Kidney international, 70 (12), 2074-84 PMID: 17063179

Menke, A. (2006). Blood Lead Below 0.48 mol/L (10 g/dL) and Mortality Among US Adults Circulation, 114 (13), 1388-1394 DOI: 10.1161/circulationaha.106.628321

Schnaas, L., Rothenberg, S., Flores, M., Martinez, S., Hernandez, C., Osorio, E., Velasco, S., & Perroni, E. (2005). Reduced Intellectual Development in Children with Prenatal Lead Exposure Environmental Health Perspectives, 114 (5), 791-797 DOI: 10.1289/ehp.8552

Schwartz, B., & Stewart, W. (2007). Lead and cognitive function in adults: A questions and answers approach to a review of the evidence for cause, treatment, and prevention International Review of Psychiatry, 19 (6), 671-692 DOI: 10.1080/09540260701797936

Cecil KM, Brubaker CJ, Adler CM, Dietrich KN, Altaye M, Egelhoff JC, Wessel S, Elangovan I, Hornung R, Jarvis K, & Lanphear BP (2008). Decreased brain volume in adults with childhood lead exposure. PLoS medicine, 5 (5) PMID: 18507499

Hauser, R., Sergeyev, O., Korrick, S., Lee, M., Revich, B., Gitin, E., Burns, J., & Williams, P. (2008). Association of Blood Lead Levels with Onset of Puberty in Russian Boys Environmental Health Perspectives, 116 (7), 976-980 DOI: 10.1289/ehp.10516

Jusko TA, Henderson CR, Lanphear BP, Cory-Slechta DA, Parsons PJ, & Canfield RL (2008). Blood lead concentrations Environmental health perspectives, 116 (2), 243-8 PMID: 18288325

Wright JP, Dietrich KN, Ris MD, Hornung RW, Wessel SD, Lanphear BP, Ho M, & Rae MN (2008). Association of prenatal and childhood blood lead concentrations with criminal arrests in early adulthood. PLoS medicine, 5 (5) PMID: 18507497

Iqbal S, Blumenthal W, Kennedy C, Yip FY, Pickard S, Flanders WD, Loringer K, Kruger K, Caldwell KL, & Jean Brown M (2009). Hunting with lead: association between blood lead levels and wild game consumption. Environmental research, 109 (8), 952-9 PMID: 19747676