Monday, 8 July 2013

Humans vs Tigers

I have been following an interesting news of a match of Humans vs Tigers. The eventual outcome was a draw: one man and a tiger cub killed on each side.

 The story is that six men from Simpang Kiri village in Aceh Tamiang district went to the Mount Leuser National Park on Sumatra Island for harvesting agarwood (used in incense and perfume). I am assuming that this was probably illegal since national parks does have restricted entry and harvesting this precious material is probably regulated. Nonetheless, they set traps to catch deer (again, I am unsure about whether this amounts to poaching) and caught a Sumatran tiger (Panthera tigris sumatrae) cub instead (which eventually died). This action attracted 5-7 tigers in the vicinity who, quite notably, chased the men. The men climbed up some trees and hung on to dear life for five days, subsisting on rainwater. The tigers, equally persistent, remained at the base. One man was mauled to death when he fell down after a branch snapped. The others contacted nearby villagers via the cell phones. The villagers were helpless, but eventually "tamers" and the rescue team drove the tigers away.

 I could debate at length about whether the men deserved the plight they faced, but more interesting is the behaviour of the tigers. The Sumatran tiger is the smallest (75-140 kg - Prothero et al, 2012) and is critically endangered (Sunarto et al, 2013). It is endemic to, well, Sumatra and the population is around 350. The low numbers are due to deforestation and conversion of lands into acacia and oil palm plantations, fires, and poaching (O'Brien et al, 2003; Sunarto et al, 2012; Johnson, 2013) . This plight was recently highlighted by Sunarto et al, 2013, who calculated that numbers were much lower in the Riau province which was believed to have the highest concentration of tigers (Banerjee, 2012, state that the population had declined by 70%; from 640 in 1982, the numbers fell to 192 in 2007). In a previous paper, the same authors proved that tigers are not particularly fond of plantations and settlements, preferring large contiguous and undisturbed forests and higher altitudes. However, the authors also encourage using the plantations as "corridors, stepping stones, or mosaics of connectivity facilitating animal movement"- which, in my humble opinion, is a recipe for disaster for both tigers and humans.

Indeed, it is sad that a human life and a tiger life were lost. But it could have gone in a few different ways. Five other humans could have been killed. So could have 5-6 critically endangered tigers. We very seldom recognise how our lifestyle preferences (I too have found agarwood to be particularly heady) might be only aggravating human-animal conflict elsewhere...

 Image source:

References Kimberly Elizabeth Johnson (2013). Living Off the Fat of Another Land: Trans Fat Social Policy and Environmental Externalities Environmental Policy is Social Policy – Social Policy is Environmental Policy, 37-50 DOI: 10.1007/978-1-4614-6723-6_4  
Timothy G. O'Brien, Margaret F. Kinnaird, Hariyo T. Wibisono (2003). Crouching tigers, hidden prey: Sumatran tiger and prey populations in a tropical forest landscape Animal Conservation, 6, 131-139 DOI: 10.1017/S1367943003003172
Donald R. Prothero, Valerie J. Syverson, Kristina R. Raymond, Meena Madan, Sarah Molina, Ashley Fragomeni, Sylvana DeSantis, Anastasiya Sutyagina, Gina L. Gage, Size and shape stasis in late Pleistocene mammals and birds from Rancho La Brea during the Last Glacial–Interglacial cycle, Quaternary Science Reviews, Volume 56, 21 November 2012, Pages 1-10, ISSN 0277-3791,

Sunarto Sunarto, Marcella J. Kelly, Karmila Parakkasi, Sybille Klenzendorf, Eka Septayuda, & Harry Kurniawan (2012). Tigers Need Cover: Multi-Scale Occupancy Study of the Big Cat in Sumatran Forest and Plantation Landscapes PLoS One DOI: 10.1371/journal.pone.0030859  

S Sunarto, Marcella J. Kelly, Sybille Klenzendorf, Michael R. Vaughan, Zulfahmi, M.B. Hutajulu, & Karmila Parakkasi (2013). Threatened predator on the equator: multi-point abundance estimates of the tiger Panthera tigris in central Sumatra Oryx, 47 (2), 211-220 DOI: 10.1017/S0030605311001530

Tuesday, 5 February 2013

Automobile exhausts and heart disease: Is the link an inflammatory molecule?

A recent study in America found evidence for increased levels of IL-1 beta,  a marker associated with inflammation in the blood of people who lived near the highways and had high exposures to vehicular exhausts.

As our consumption and usage of vehicles increases, our roads constantly brew  more particulate matter, black carbon, nitrogen dioxide, sulphur-di-oxide and carbon monoxide, all emitted from automobile exhausts. The danger about these emissions is that they don’t just stay there, but drift. Our busy highway and motorways, which have high traffic volume, are the worst offenders. Studies indicate that people living/working in such areas and spending significant time within approximately 200m of highways are exposed heavily to these pollutants compared to people who are based further away. Unsurprisingly, the exposures at highways are higher when compared to people living on busy urban streets.

A plethora of studies have linked vehicular emission exposure to heart disease. We had highlighted a couple of them in this blog. The closer people live or work near highways/motorways, the greater is their exposure to the  harmful effluents.  However, many of the studies in this field  of research are epidemiological in nature which are population based and  subject to the criticism that the observed correlation in the studies might not really signify causality. A recent study by researchers from Tufts School of Medicine, Boston, attempts to close the gulf and provides a molecular basis of the effects of vehicular emission exposure on human health and offers an explanation on how automobile exhausts could cause heart diseases. 

The study was conducted in the  Somerville area of  Massachusetts, USA.  The scientists compared blood samples from 20 people who lived less than 100m from the Interstate-93( a highway that connects Massachusetts to Vermont) and those residing a km away from the highway in urban backgrounds. To ensure that the  two groups were as  similar as possible,  the subjects in both groups were matched to age, gender and education. Though there were no significant differences between two groups in terms of body measurements (height, weight) and education, the group who lived in urban backgrounds were more likely to earn less, had higher exposure to vehicle exhausts that was occupationally related and high levels of bad cholesterols (LDL). The researchers factored the job related vehicle emission exposure in their calculations and found that the levels of IL-1 beta was increased significantly in those people who lived near the highway.

Inflammation plays a crucial role in the development and progression of a variety of heart diseases importantly atherosclerosis and congestive heart failure.  Inflammatory molecules linked to these processes includes interleukin-1 (IL-1), but this American study  is the first of its kind where such a link has been shown to occur  in humans with proximity to heavy traffic. The results are notable as it also recapitulates the trend shown by particulate matter  in increasing the  levels of   IL -1 family  in  animal models and cells in culture. In their paper, the researchers also point out that  IL-1 beta itself could have application as a biological marker of air pollution exposure. However, one thing to note is that  IL-1 family is also influenced by diet and this is a factor that has to be controlled for in further experiments. Cumulatively, the study by Professor Brugge and his colleagues  is a very interesting preliminary work which warrants larger carefully controlled follow up studies.

Fearon, W., & Fearon, D. (2008). Inflammation and Cardiovascular Disease: Role of the Interleukin-1 Receptor Antagonist Circulation, 117 (20), 2577-2579 DOI: 10.1161/CIRCULATIONAHA.108.772491 Brugge, D., Durant, J., & Rioux, C. (2007). Near-highway pollutants in motor vehicle exhaust: A review of epidemiologic evidence of cardiac and pulmonary health risks Environmental Health, 6 (1) DOI: 10.1186/1476-069X-6-23 Brugge, D., Lane, K., Stewart, A., Tai, A., & Woodin, M. (2013). Highway Proximity Associations with Blood Markers of Inflammation: Evidence for a Role for IL-1β Journal of Toxicology and Environmental Health, Part A, 76 (3), 201-205 DOI: 10.1080/15287394.2013.752325

Wednesday, 30 January 2013

Pussy Cat, Pussy cat, what have you killed?

In the early eighties, our parents rescued two abandoned stray kittens from the road, which started a long line of cat dynasty in our house and the neighbourhood. Our house gained the reputation of being a sanctuary for abandoned cats, that we had people stealthily abandoning their cats outside our house gates. At one point, we had about 12 cats in the house. We loved these animals dearly; but despite being fed adequately, we were horrified to note that they killed squirrels, birds, bats, bandicoots, rats and mice. We lamented their notorious habit of murdering birds and squirrels, particularly as we fed them too, and could never comprehend how our adorable pets could turn into merciless masochistic killers, particularly as they never ate their kill. The carcass was presented for us to see almost very time.  I remember one time when my mother was inconsolable, when a cat killed one of ‘her’ doves that she had grown so attached to. Our repeated efforts to teach the cats 'good behaviour' was not fruitful.  

The  results presented in recent paper in Nature Communications by Loss and his colleagues on the 'The impact of free-ranging domestic cats on wildlife of the United States' was not a surprise in one respect ,as we all know that cats kill birds and smaller mammals. However, what was surprising was the magnitude of the effects. Domestic cats have been introduced globally by man and are linked to the extinction of several animals on islands, whilst their effect on other places had not been scientifically estimated. In their study, the authors estimate that in the US, domestic cats alone kill 1.4-3.7 billion birds and 6.9-20.7 billion mammals every year, and that cats that are not owned (feral cats) as opposed to owned pets, cause the majority of the killing. What is different about the study when compared to previous ones, is the actual quantification the authors conducted, which suggest that cats cause significant and substantial wildlife mortality than previously thought. Interestingly, these cute and cuddly creatures which are the most popular pets in the world are the primary and greatest source of anthropogenic (caused by humans- in this case indirectly) mortality for US birds and mammals. This makes me wonder, whether their new found notoriety would affect their popularity as pets. For some reason, I doubt it.

2. Loss, S., Will, T., & Marra, P. (2013). The impact of free-ranging domestic cats on wildlife of the United States Nature Communications, 4 DOI: 10.1038/ncomms2380

Sunday, 20 January 2013

Snow in Britain

Britain has had an onslaught of snow since last Friday. Here are some snaps from the Midlands.

Saturday, 19 January 2013

A dangerous cocktail brews in our towns and cities- How tobacco smoke and vehicular emissions together contribute to wheezing in young children

Vehicular emissions and tobacco smoke are harming the lungs of young children  in our cities

When it comes to the evidence against tobacco and vehicular emissions on harming human respiratory health, it does not rain but it pours. And it keeps on coming. We have extensive evidence to show that vehicular emissions as well as tobacco smoke exposure are bad for health and it seems to start right from the fetal stage.  A new study presented in the journal Environmental Health shows that exposure to traffic-related air pollutants is associated with increased risks of wheezing in children who are exposed to tobacco smoke in fetal  life and infancy indicating an axis of villains who co-operate to exert their  harmful effects.

The study was a large prospective cohort study involving 4,634 children in Rotterdam, the second largest city in the Netherlands.  One of the largest ports in the world, it is also one of the most polluted places in the Netherlands and an apt location for pollution studies. A prospective cohort study is one that monitors a group of similar individuals –cohorts- who differ in certain factors under study over a time period in order to understand how these factors affect rates of a certain outcome- in this study, how effects of vehicular emissions, tobacco smoke exposure (in any stage starting from fetal life to the age of 3 years) affect wheezing in children.

Many cities, like this one, has air pollution monitors that helps scientist understand how air pollutants affect human health .
 Particulate matter (PM) of the size of 10 microns or less can penetrate the deepest part of the lungs such as the bronchioles or alveoli. Domestic coal combustion was once the major source of particulate emissions, but recently other sources such as road transport are important sources with diesel vehicles notably emitting increased levels. Road vehicle exhausts, off road equipment, and power plants  are  important sources of NO2.  In addition to contributing to the formation of ground-level ozone, and fine particle pollution, NO2 is linked with a number of adverse effects on the respiratory system. In this study, the exposure of children to particulate matter (PM10) and nitrogen dioxide (NO2) were assessed by analysing emission data at the home address. Parents were asked to fill questionnaires that indicated whether their children had wheezing until the age of 3 years.  Parents were also asked to provide information on whether the fetus or the baby had been exposed to tobacco smoke either through the mother or the partner smoking tobacco.

Results from the study indicated that average annual PM10 or NO2 exposure levels per year were not associated with wheezing in the same year.  Even though there were trends showing a link with PM10 or NO2 exposure levels and wheezing during the first 3 years of life, the results were not statistically significant. The researchers did not observe associations of traffic-related air pollutants with wheezing among children who were exposed to smoke during fetal life only or during infancy only. But in children who were exposed to tobacco smoke in both fetal and infant stage, PM10 or NO2 exposure levels was associated with wheezing during the first 3 years of life. The scientists did not observe associations of traffic-related air pollutants with wheezing among children who were not exposed to tobacco smoke.

There are limitations in the study, one of  which the researchers have noted viz. the possibility of ‘misclassification of air pollution assessment’ owing to the analysis only  involving  exposure levels at home addresses and not at the day care centers or other places where the child may spend days and nights. One factor that could have further added value to the study is blatantly missing- work addresses of mothers and PM 10, NO2 levels  - and whether when analysed together with air pollution exposure at home had any links to wheezing in children.

Nevertheless the study extends our understanding on how air pollution and tobacco smoke exposure contribute to the health of younger children. The  results suggest that long term exposure to traffic-related air pollutants is associated with increased risks of wheezing in children exposed to tobacco smoke in fetal life and infancy. Tobacco smoke exposure in early life might lead to increased vulnerability of the lungs to air pollution. The evidence appears to show that exposure of fetus and  infant lung to tobacco smoke primes it for damage by air pollutants leading to wheezing suggesting that the dangerous cocktail is made more potent by the ingredients together.


Sonnenschein-van der Voort, A., de Kluizenaar, Y., Jaddoe, V., Gabriele, C., Raat, H., Moll, H., Hofman, A., Pierik, F., Miedema, H., de Jongste, J., & Duijts, L. (2012). Air pollution, fetal and infant tobacco smoke exposure, and wheezing in preschool children: a population-based prospective birth cohort Environmental Health, 11 (1) DOI: 10.1186/1476-069X-11-91

Wednesday, 9 January 2013

Exposure to air pollutants during pregnancy linked to autism in children

Vehicular air pollution could cause autism - Photo by Sarah Stephen

A recent study by Californian researchers indicates increased odds for developing autism in children whose mothers were exposed to ozone and particulate matter 2.5 (PM2.5). Ozone and PM2.5 are associated with vehicular pollution and this study emphasizes the dangers posed by traffic pollutants to health in utero.

The researchers used Los Angeles as a sample population. Mothers of over 7600 children between ages of 3-5, diagnosed with autism during 1998-2009, were identified and their addresses at the time of pregnancy established. For each case, 10 controls were used in the analysis, and the addresses of the mothers were linked with air monitoring stations in the vicinity. The researchers then used using data from air monitoring stations and a land use regression (LUR) model to estimate exposures and came to the conclusion that ambient air pollution is linked to autism. Though LA is much cleaner than it used to be, it frequently has the highest levels of ozone within the country. According to the authors, theirs is the first study to show a link between autism and ozone.

With the increase in the prevalence of autism in the recent years, such an association is of relevance, yet calls for further detailed and stringent studies. Exposure to air pollutants in pregnant mothers has been linked to several diseases in children. In fact, a previous study  linked ambient concentration of solvents and heavy metals near maternal residences to autism in children. The findings of the recent study cannot be taken lightly. However, the problem with many population based studies is that an association doesn't always signify causality, an argument touted by skeptics, and often the hardest to prove otherwise.

Becerra, T., Wilhelm, M., Olsen, J., Cockburn, M., & Ritz, B. (2012). Ambient Air Pollution and Autism in Los Angeles County, California Environmental Health Perspectives DOI: 10.1289/ehp.1205827

Windham, G., Zhang, L., Gunier, R., Croen, L., & Grether, J. (2006). Autism Spectrum Disorders in Relation to Distribution of Hazardous Air Pollutants in the San Francisco Bay Area Environmental Health Perspectives, 114 (9), 1438-1444 DOI: 10.1289/ehp.9120


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