It is known that smoking causes lung cancer and heart disease. Does smoking play a role in causing colorectal cancer (CRC)? While there are well known genetic causes for CRC, most CRCs in the general population are not genetically linked. Colonic adenomatous polyps are precursors to CRC; the larger the polyp, the higher the chance that it will have malignant potential. Colorectal polyps can be pedunculated or flat. Pedunculated polyps are easier to visualise and flat polyps can be missed easily during colonoscopy, especially when they are small. If adenomatous polyps are left untreated, they will turn into colon cancer with time. Recently, the American College of Gastroenterology published guidelines suggesting that smokers with a history of > 20 pack years may need screening for CRC earlier than their non-smoking counterparts. Are smokers at higher risk of developing colon polyps?

Researchers from Seoul National University Hospital studied 5254 asymptomatic subjects undergoing screening colonoscopy (J Gastroenterol Hepatol 2010; 25: 519 – 525). They were split into 3 groups aged 30 – 39 years, 40 – 49 years and 50 – 59 years. The prevalence of overall adenomas was 10.4% in the 30- 39 years age group, 22.2% in the 40 – 49 years age group and 32.8% in the 50 – 59 years age group. The prevalence of advanced adenoma was 0.7%, 2.7% and 4.1%, respectively. Male sex, current smoker and family history of CRC were independent predictors of advanced adenoma in the 40 - 49 years group. The risk of developing advanced adenoma in smokers is increased by 58%.

In another study from the University of Connecticut, 600 asymptomatic patients presenting for CRC screening were studied with high-definition colonoscope to detect flat adenomas (Gastrointest Endosc 2010; 71: 1234 – 1240). Of these 600 patients, 313 were non-smokers, 115 were heavy smokers (10 or more pack years and still smoking or had quit within 10 years) and 172 were low-exposure smokers (< 10 pack years or had quit more than 10 years ago). Heavy smoking increased the risk for flat adenomas of any size by 153%. The risk for flat adenomas of 6 mm or more was increased 284% in heavy smokers. Heavy smoking increased the risk of advanced flat adenomas by 181%. How heavy you smoke also increased the risk of developing flat adenomas. The risk was increased 128 % in those with > 30 pack years of smoking compared to those with < 30 pack years.

Smoking is known to cause many health problems. It is also considered to be an anti-social behaviour by many. Yet the number of smokers worldwide is increasing, especially in developing and under-developed countries. The mind boggles!

Being obese is known to be associated with increased health problems. These include diabetes, heart diseases, sleep apnoea and joint problems to name a few. It is also known that obese women have an increased risk of breast cancer. Is this association true for other cancers too?

Researchers from several universities from both sides of the Atlantic analysed the pooled data from the National Cancer Institute Pancreatic Cancer Cohort Consortium (PanScan) to look at possible association between obesity and risk of pancreatic cancer. The study included 2170 cases of pancreatic cancer and 2209 controls (Arch Intern Med 2010; 170: 791 – 802). They recorded body mass index (BMI) [< 18.5 underweight, 18.5 – 24.9 normal weight, 25.0 – 29.9 overweight, 30.0 – 34.9 obese and 35.0 severely obese], waist circumference and waist to hip ratio. In men, the risk of pancreatic cancer in those with the highest quartile of BMI is increased by 33% as compared to those with the lowest quartile BMI. In women the increased risk is 34%. An increased waist to hip ratio, between the highest and lowest quartile, was also associated with an 87% increased risk of pancreatic cancer in women.

We have two types of cholesterol in our body: ‘good’ cholesterol, namely high-density lipoprotein cholesterol (HDL-C), and ‘bad’ cholesterol called low-density lipoprotein cholesterol (LDL-C). We know that people with adequate levels of HDL-C are protected from heart disease. Does having more good cholesterol also protect you from cancer?

Researchers from Tufts University in Boston, USA, examined the relationship between HDL-C levels and the risk of developing cancer in 24 large randomised controlled trials (RCTs) of lipid-altering interventions (J Am Coll Cardiol 2010; 55: 2846 – 2854). The study found that there was a significant inverse association between baseline HDL-C levels and the rate of incident cancer. In other words, the higher the HDL-C level, the lower is the risk of cancer. After controlling for variables such as LDL-C level, age, BMI, sex and smoking status, the study found that for every 10 mg/dL increase in HDL-cholesterol, there is a 36% lower risk of developing cancer.

Most individuals put on weight because they eat more than they need. Whether you manage to lose weight or not depends on your motivation and determination. Participants in the reality show ‘The Biggest Loser’ manage to lose significant amounts of weight because they are being motivated to do so. Not everyone will get the chance to go on the show in order to be motivated. However, is the knowledge that becoming obese will increase your risk of developing cancer not enough to motivate you to keep trim?

Residents of a condominium or housing estate in Singapore scurry to close all their windows when they hear “Brrrrrr ….” outside their flat or house. This is the familiar sound of the machine which spews out a thick cloud of insecticide to kill mosquitoes or bugs in the compound. When the dense white cloud has dispersed, the air is still laced with the lingering smell of chemicals for some time. I have always wondered what health hazard this fogging / fumigation poses.

A recent article titled “Residential and childhood leukemia: A systematic review and meta-analysis” written by researchers from the University of Ottawa caught my eye (Environmental Health Perspectives 2010; 118: 33 – 41). They reviewed and analysed previously published epidemiological studies examining the relationship between residential pesticide exposure during critical exposure time windows (preconception, pregnancy and childhood) and childhood leukaemia. The analysis found a positive association of exposure and childhood leukaemia. During pregnancy, exposure to unspecified residential pesticides, insecticides and herbicides carried 54%, 105% and 61% increased risk of childhood leukaemia, respectively. During childhood, exposure to unspecified residential pesticides and insecticides carried 38% and 61% increased risk of childhood leukaemia, respectively.

Most childhood leukaemia occurs in the first few years of life. Most leukaemics carry gross chromosomal abnormalities in their blood. A study in the late 90s on routinely collected blood samples in neonates showed the presence of leukaemic clones with specific chromosomal translocations in children who later developed acute lymphoblastic leukaemia (ALL) [Proc Natl Acad Sci USA 1997; 94: 13950 -13954]. Another study suggested that pre-leukaemic clones may persist throughout childhood and may require post-natal exposure for leukaemic progression (Genes Chromosomes Cancer 2004; 39: 335 – 340). A recent study of infants born in an agricultural region in the Philippines showed that the prevalence of a common acute myologenous leukaemia (AML) translocation [t(8;21)] in cord blood samples was about doubled in those infants with detectable meconium levels of the methylcarbamate insecticide propoxur (Pediatr Blood Cancer 2007; 49: 624 – 628).

Leukaemia is the most common form of childhood cancer in Canada and the United States. ALL accounts for about 80% of childhood leukaemic cases. The next most common is AML. Although the precise mechanism on how leukaemia develops is still unclear, the two-step leukaemia model proposes that leukaemia development occurs after 2 mutations. The first mutation, usually a chromosomal translocation, occurs in utero. The second mutation, occurring after birth, completes the process and leukaemia occurs. While ionizing radiation is the only proven environmental risk factor to play a role in the etiology of leukaemia, other potential risk factors include parental smoking and alcohol consumption, electromagnetic field exposure, hydrocarbons, socioeconomic factors, immunity and infection and pesticides.

While it has not been convincingly proven that pesticides / insecticides cause leukaemia, it is probably no harm that we avoid unnecessary exposure to these substances as much as possible. While fogging / fumigation helps to reduce the mosquito population, it may bring nastier problems in its place to you and your family.