Evidence-based Review of Cancer Due to Household and Occupational Chemical Exposure.

Posted in Uncategorized on July 23, 2010 by theseep

Clint Slaughter, M.D

February 15, 2008

Walden University Master’s of Public Health Program


Cancer of all types is a major public health problem that despite public health campaigns, is still growing in new  and concerning ways.  In our modern industrialized society, on a daily basis we are exposed to countless chemicals, toxins, and carcinogens in the form of fumes, preservatives, pesticides, fertilizers, waste runoff, and residues. Some of these substances have been proven to be harmful, some of them are speculated to be harmful, and for many of them, we have no idea as to their potential impact on our health. Even though we are certain of many of these health effects, the offending chemicals are still in our everyday foods, packaging, toys, household cleaners, household pesticides, building materials, and many other products.

Media attention has been increasingly drawn to human disease as a result of these types of chemical exposure, seen recently with Melamine tainted milk and eggs from China, lead in children’s toys, and the FEMA trailer debacle where hundreds of people became ill due to high levels of formaldehyde in the trailers used for disaster victims (Final Report on Formaldehyde, 2008). It is frightening to note that the very same building materials used in these types of trailers, which off-gas VOCs (volatile organic compounds) such as formaldehyde, are used in a wide array of home furniture products and home construction and have been for years (Tox Town, 2008). Recently, the safety of Bisphenol A, a chemical found in many plastic water bottles, food containers, and the lining of many tin cans, has finally been brought to the public’s attention. More and more of these issues will arise as the environmental concentration of these chemicals increase and more health problems are seen as a result. Some of these exposures cause vague symptoms, others cause identifiable toxidromes, and others have been shown to be carcinogenic. There are a number of studies that demonstrate cancer directly attributable to preventable exposures, most notably lung cancer from smoking and second hand smoke exposure (Centers for Disease Control, 2007). There is direct evidence for childhood leukemia caused by exposure to household solvents and pesticides (Freedman, Stewart, Kleinerman, Wacholder, Hatch, Tarone, et al, 2001), (Buckley, Robison, Swotinsky, Garabrant, LeBeau, Manchester, et al, 1989), and increased incidence of breast cancer has been linked to a variety of exposures, including hormonally active chemicals (Davis, Bradlow, 1995).  A new report in the International Journal of Occupational and Environmental Health that focuses on breast cancer discusses the many proven and likely environmental contributors to developing the disease, such as ionizing and non-ionizing radiation, chemical exposure from air contaminants, pesticides, plastics, household cleaning products, hormones in meat and milk, cosmetics, personal care products, as well as occupational exposures (Nudelman, et al., 2009).  What seems to be an emerging theme in modern chemical exposure is the hormonally active and endocrine disrupting nature of many ubiquitous chemicals, such as Bisphenol A, phthalates, dioxins, many types of pesticides,VOCs, perchorates, diethystilbestrol (DES) , and many others.  Because so many of these chemicals, which are present throughout our homes, foods, personal care products, work in a similar fashion on the body’s endocrine and hormonal systems, there is undoubtedly an additive effect which is very difficult to quantify(Nudelman, et al., 2009).  Since correlations have been made individually between these many chemicals and cancer or other illnesses, this has set the stage for the next generation of studies to further investigate and find stronger causal relationships as well as look at the additive and temporal effects of these exposures.

The population affected by this issue is broad, essentially any consumer that purchases products for their home, those purchasing processed and packaged food products and containers, as well as those working in industry with chemical exposures. Household chemicals in some way affect every person. There may not be overt symptomatology, but physiologic changes take place on a low level, increasing the risk for various types of cancers and disease processes. In certain professions, such as refining and farming, exposures to carcinogens are the norm.

This problem effects us all in varying levels, but can disproportionally effect those living in areas with concentrated levels of certain chemicals, those that regularly utilize potentially hazardous products, and especially those in developing nations where many modern potentially hazardous substances and products are produced or disposed of.  Children, pregnant women, and the elderly are also at greater risk for developing disease from lower levels of exposure (Freedman, et al, 2001).  Shifts in exposure can occur quickly as well, as in the aftermath of Hurricane Katrina, where thousands of people were displaced from their homes and many were provided trailers to live in by the Federal Emergency Management Agency (FEMA).  It was found later that these trailers, made from standard off-the-shelf building materials, were off-gassing enough volatile organic compounds (VOCs) such as formaldehyde to cause significant health problems in many of those living in them (Final Report on Formaldehyde, 2008). Although it was dismissed by some, offering that these types of trailers were not meant to live in for prolonged periods, these very same materials such as pressboard, melamine, paints and sealants, are used in regular home construction as well and can affect any homeowner given the proper concentrations and conditions.

The true prevalence of illness as a result of low-level chemical exposure in the home or at work is unknown and is anticipated to be highly variable depending on socioeconomic status, location, and profession.  Some of the more obvious and longstanding exposures such as cigarette smoke exposure have excellent data to support a strong causal relation.  From extensive studies, we know that smoking can be blamed for 80% of lung cancers in women and 90% of lung cancers in men (Centers for Disease Control, 2007).  Even though the prevalence and risk of chronic low-level exposures is unknown, the significance is great. In recent years, we are seeing more and more evidence of illness as a result of exposure to chemicals that are either unregulated or are approved by our government to be used without proper testing.


This ubiquitous public health issue is similar to many in that not only can individual education and change play a large role, but enacting policy and political change is also an imperative part of the process towards better safety.  In order to make changes in an individual’s behavior, many facets must be addressed and using behavioral theories to analyze actions and tailor education and programs is essential.  Because long-term exposures do not have much, if any, short-term feedback to the individual, some models such as the stages of change theory or the social learning theory are less applicable.  Because it is important to emphasize the perceived dangers of long-term exposures as well as generate a shift in acceptable industry standards, the Health Belief model, Consumer Information Processing model, or Theory of Reasoned Action could all be applied to the problem (Schneiderman, N., et al, 2001).

First, however, we must explore what it is that most effects a consumer’s decision making process to buy one product over another.  Again, because of the insidious and largely unknown long-term effects of exposures to toxic chemicals, it is more challenging to convince an individual of direct risk.  When a person feels the negative effects of an action directly, it is easier to change behaviors to avoid these effects. However, for long-term and low-level chronic effects, it is much more difficult to motivate a change.  An example is daily caloric consumption.  Because weight gain is a slow process, eating a small amount of excess calories a day may cause a 10 pound weight gain over a year or more. It is difficult to make meaningful alterations in our diet when we do not see the immediate effects of the behavior.  Another very strong behavioral factor in the reluctance to move from the current potentially toxic consumption to healthier alternatives is cost.  Over the last century as manufacturing techniques have evolved and we have seen globalization of markets and production, there has been strong corporate pressure to decrease costs to be more competitive.  This pressure commonly causes something important to be cut from the process, be it proper waste disposal leading to environmental contamination, dangerous or oppressive working conditions, inferior materials used that are potentially toxic, and other money-saving tactics that tend to increase the risk to consumers but at the same time bringing the cost to consumers down and increase the profit margins for the manufacturer.  In a 2008 Gallup poll, it was found that with the economic downturn, 81% of those asked made more of an effort to find the cheapest price of a product and 49% switched to lower quality products due to cost (gallup.com, 2008).  This confounds efforts further in that if the perceived danger of an exposure to a product is low, and true environmental and societal costs of a product are not considered, most consumers will choose based on cost.  When faced with the gluttony of products available, often with confusing or inadequate labeling and unintelligible chemical names, and no warnings of potential hazards, it is no wonder that consumers often ignore the content, manufacturing techniques, or origin of products, instead looking for function and low cost.

From a psychosocial aspect, many factors play a role in consumer behaviors aside from the effects on the individual and their wallets, people are products to a significant extent of their environment and are influenced greatly by social perceptions and social norms.  Our status quo places a great deal of trust in our retail system despite the fact that it is so poorly regulated.  Consumers assume that if a product is on the shelves to be purchased, it is safe to use, and because many exposure-related illness cannot be traced back to a single product, there is little motivation to pursue a social change for many.  Our consumerism has become so ingrained in our society through psychological advertising of products and the immersion of our culture in media, that a mistrust of everyday products, manufacturing methods, and “traditional” farming methods with pesticide, is often looked upon with disdain and dismissed as odd or irrational.  Since it is the norm to use toxic household cleaners, pesticides, and building materials, there is no social motivation to make a change.  Also, within a person or family’s social support groups, there is often little or no knowledge of issues with household chemicals aside from single-incident poisoning risks and therefore no impetus to seek out information on the dangers of chronic exposures. This disconnect between each individual consumer purchase and the trail of toxins, societal and environmental costs, and potential health threats that lie behind that purchase have reached a dangerous tipping point.  In order to counteract the unfounded consumer trust and the obliviousness to these true costs, consumer education and community action are needed.


There are already a number of public health initiatives designed to educate about poisoning episodes, where a child or family member accidentally drinks or is exposed to a hazardous substance in the home. The CDC has National Poisoning Prevention Week (Center for Disease, 2008), and the National Department of Health Services has “Poison Help”, a program to educate consumers on poisonings, hazardous chemicals, and how to seek proper treatment.  However, education on how toxic many of the substances in our own homes and suitable, safe alternatives is lacking.  We have also seen extensive and successful campaigns for breast cancer awareness that educate on the many environmental contributors to breast cancer.  These types of grass-roots campaigns can very effective in engaging the public to take action that can then spur political and policy change.

At present there are multiple government agencies that have responsibilities in recognizing disease patterns and regulating exposures, including the Centers for Disease Control, the Food and Drug Administration, Department of Health and Human Services National Toxicology Program, the Consumer Product Safety Commission, and the Environmental Protection Agency.  It seems that all of these departments have educational materials on hazardous products, but aside from the acute poisoning programs mentioned above, there are as of yet no major public health programs to educate consumers on product and exposure safety.  These agencies are still operating on a “damage control” philosophy, where action is taken on an individual product or health concern when people actually start to become ill.  Even with the proven problems from VOCs like formaldehyde with the Katrina trailers and the multiple cases of lead exposure and melamine contamination over this past year, we have yet to see any meaningful legislation to prevent this from happening in the future.  Many of the aforementioned grass-roots organizations do seek to educate the public and instigate change, but many offer anecdotal evidence and supposition rather than peer-reviewed literature to support claims.  Unfortunately there is a paucity of adequate research on the additive effects and long-term exposure risks of most of what we are exposed to today, and by making some untrue or sensationalist claims, even in the midst of legitimate data, these types of grass-roots efforts tend to undermine their own credibility.  This is why it is imperative for these governmental agencies to take a more active and organized role to prevent cancer and other human health problems as a result of environmental exposures.


In order for government agencies to begin the necessary regulation, essentially a revamping of our entire screening and approval processes for consumer goods and industrial safety exposures is required.  We are already years behind European countries in outlawing various hazardous chemicals, and the integrity of our process needs to be reviewed, removing influence from companies and lobbyists that purposely present biased data or hide known hazards.  The major paradigm shift will be that rather than approve until proven harmful, our system should disallow until proven safe.

The current system utilizes the quantitative risk assessment model, meaning that chemicals can be produced and products brought to market without any safety assessments. If any human health problems result from use or exposure to these substances, the onus is on the consumer or regulatory bodies to “scientifically” prove that harm is present before a product is discontinued (Cohen, Chavez, Chehimi, 2007). This system puts the advantage squarely in the hands of industry, making it very easy to produce and sell untested goods, but making it very difficult to have a product removed from store shelves or taken out of production. What makes the process even more difficult and less safe for consumers is that the health effects of low-level, long-term exposure to many chemicals is insidious and often nearly impossible to determine a definite cause.  This is further confounded by the ubiquitous nature of our current industrial chemical exposure, with additive exposures from multiple sources or from chemicals with similar physiologic effects as we see with the many hormonally active substances discussed previously.  To make matters worse, those with lower socio-economic status are often exposed to higher concentrations of toxic substances and although they are disproportionally affected, they have less access to healthcare as well as less of a voice to initiate change in the status quo (Cohen, et al, 2007).

One of the most effective policy changes that can be made to protect consumers over industry is to shift from the quantitative risk assessment model to the precautionary principle when dealing with chemicals and consumer goods. The precautionary principle basically means that products should be shown to be safe prior to exposing the public to them, rather than proving harm once effects are seen. It also places the financial and legal burden on the manufacturer rather than the public. Interestingly, the 1999 White House Policy Declaration on Environment and Trade “acknowledges that a precautionary approach is an essential element of the U.S. regulatory system (Cohen, et al, 2007) yet there has not been any meaningful change in policy or approach to the rising reports of exposure-related illness.  The other major policy change needed is to initiate mandatory labeling requirements of products to include warnings of potential toxic effects, similar to cigarette packages.  By requiring the labeling of all products with potentially hazardous substances, consumers will have more data on hand to make informed decisions when purchasing products.

Many industry advocates complain that by increasing testing and regulation of products and changing labeling requirements will drive up costs to consumers.  Although this is true to some extent, from a public health perspective there would be significant resultant savings in healthcare costs from reduced illness secondary to exposure.  Unfortunately, as with many public health issues, these types of healthcare cost savings are impossible to accurately predict and therefore are often not given serious consideration.  Unfortunately, the costs of many of the products we buy and consume are artificially and underhandedly lowered by cutting corners with labor laws, waste disposal and the raw materials used, and it is natural for costs to go up when social justice, health, and environmental sustainability are brought into play.

By engaging and educating the public on the toxic nature of many of the everyday chemicals we are exposed to, and by forcing manufacturers to properly test and label their products, we will see a shift in consumer habits and a decrease in related disease states that we see today as well as those that we will uncover in the future.  Much more research and monitoring is needed to generate the proper data to fully support many of these correlations, but more studies are coming out every month that show increasing human health concerns from environmental exposures, demonstrating that policy based on the precautionary principle wise.


Abnet, C. (2007) Carcinogenic Food Contaminants. Cancer Investigation. 25:189-196

Buckley, J.D., Robison, L.L., Swotinsky, R., Garabrant, D.H., LeBeau, M., Manchester, P., Nesbit, M.E., Odom, L., Peters, J.M., and W.G. Woods. (1989). Occupational exposure of parents of children with acute nonlymphocytic leukemia: a report from the Children’s Cancer Study Group. Cancer Research. 49:4030-4037.

Centers for Disease Control (2008). Final Report on Formaldehyde Levels in FEMA-Supplied Travel Trailers, Park Models, and Mobile Homes. Retrieved on December 28, 2008 from: http://www.cdc.gov/nceh/ehhe/trailerstudy/

Centers for Disease Control (2007). Lung Cancer Risk Factors. Retrieved on January 118, 2009 from http://www.cdc.gov/cancer/lung/basic_info/risk_factors.htm

Cohen L., Chavez V., Chehimi, S. (2007). Prevention is primary: Strategies for community well-being. Jossey-Bass. San Francisco.

Davis, A. (2007) Home Environmental Health Risks. Online Journal of Issues in Nursing. 12:2. Retrieved from Academic Search Premier Database

Davis, D. (1981). Cancer in the Workplace. A Case for Prevention. Environment. 23:6

Davis, D., Bradlow, L. (1995). Can Environmental Estrogens Cause Breast Cancer? Scientific American. 273:4. Retrieved from Academic Search Premier Database

Davis, D., Muir, C. (1995). Estimating Avoidable Causes of Cancer. Environmental Health Perspectives Supplements. 8:103. Retrieved from Academic Search Premier Database

Freedman, D., Stewart, P., Kleinerman, R., Wacholder, S., Hatch, E., Tarone, R., Robison, L., Linet, M. (2001). Household Solvent Exposures and Childhood Acute Lymphoblastic Leukemia. American Journal of Public Health. 91:4

Gallup.com (2007) Surging Prices Change U.S. Consumers Behavior.  Retrieved on February 15, 2009 from:  http://www.gallup.com/poll/108892/Surging-Prices-Changing-US-Consumer-Behavior.aspx

National Institute of Health, National Library of Medicine (n.d.) Tox Town: Volatile Organic Compounds. Retrieved on October 19, 2008 from: http://toxtown.nlm.nih.gov/text_version/chemicals.php?id=31

Nudelman, J., Taylor, B, Evans, N., Rizzo, J., Gray, J., Engel, C., Walker, M. (2009) Policy and Research Recommendations Emerging from the Scientific Evidence Conneting Environmental Factors and Breast Cancer.  International Journal of Occupational and Environmental Health.  15:1

Sanborn, M., Cole, D., Kerr, K., Vakil, C., Sanin, L., Bassil, K. (2004) Systematic Review of Pesticide Human Health Effects.

Schneiderman, N et al (2001). Integrating Behavioral and Social Sciences With Public Health. Washington, DC: American Psychological Association.

Sexton, K., Hattis, D. (2007) Assessing Cumultive Health Risks from Exposure to Environmental Mixtures – Three Fundamental Questions. Environmental Health Perspectives. 115:5

U.S. Department of Health and Human Services (2008). NTP-CERHR Monograph on the Potential Human Reproductive and Developmental Effects of Bisphenol-A. retrieved on September 5, 2008 from: http://cerhr.niehs.nih.gov/chemicals/bisphenol/bisphenol.pdf

In Defense of the iPhone 4

Posted in Uncategorized on June 28, 2010 by theseep

Cracked screens.  Hard to predict crazy antenna design/ human interface signal problem.  Barely usable videoconferencing.  Oh, wait, I’m supposed to be defending it.  Defending that beautifully industrial, quirky and delicate shiny slab of glass.  That highly focused and seemingly infinite portal into communication.  I love how clear the screen is, how slim and sleek it feels in my hands. Modern, machined with precision and care.  An alluring victim of it’s own striking utility.  It mesmerizes me with it’s form, yet I know it’s only a matter of time before my slightly sweaty fingers slip and it tumbles in slow motion from my fumbling hands.  Despite the fear that makes me overgrip it’s steel edges, I marvel at it.  It can tell me anything.  I have access to so much information in a near-perfect form (aside from the almost deal-breaking and glaringly obvious oversights – I can’t videoconference anywhere except my house and effing Starbucks?  Holy crap, I’ve been wanting to videoconference on a mobile device for over a decade since I had my apple Newton!  Now it seems almost stupid idea!  Why can’t I videoconference with an iMac and why isn’t there already a Skype program?  That might start to make it useful!  I can’t even send video to an iPhone 3GS!  Are you kidding me?!  Bush league tech rollout, Steve.  Oh, wait .  . . kidding!.   . Right, I was kidding!   Seriously, those Apple videos almost made me cry.  And bringing in the deaf “I love you” at the end?  Brilliant, Mr. Jobs.  Simply Brilliant!).  The smooth, glossy glass sides absolutely terrify me.  I cradle it gently but firmly so I don’t slip and drop it, fearing that I’ll have to watch that gorgeous information portal smash, with horrific, wallet plundering, lightning bolt cracks flickering up from the pavement across that beautiful and attention-sucking Retina Display.  Destroying it forever (or until tomorrow when I blow an extra $20 for overnight shipping on a replacement screen.  Crap!  I had 8 million other things to do besides Googling “how to replace an iPhone 4 screen” and setting up my temporary amateur electronics repair shop on my messy-assed desk!).

I just checked, my bumpers won’t be here for 4 more, anxiety-provoking days.   Hrmmm. .

Right now, I usually hold  my iPhone 4 with my left thumb firmly 1/2 way down the left side, and 3 firm but deft fingers spread evenly along the right side.  Holding it this way, partly because of my terror and partly because of the reception problems, I find that I’m paying more attention to it.  The delicate yet purposeful way that my fingertips grasp the device leads me to be more conscious of my interactions with it.  Unfortunately I also almost feel like I should stick my pinky out when I’m holding it to my ear, like when pretentiously sipping tea.

I must say however, that despite the flaws, the iPhone 4 is a gloriously cool and well designed piece of genius.  Between the recharged iOS 4, the drool-inducing facade, and specifications of the device itself, it is one of the most useful pieces of communication hardware ever made.  Strong work guys.  Now get FaceTime over 3G and on iChat and Skype before I change my mind!

When are those bumpers coming in again?   I preordered an awesome bamboo case made in Oregon, but that will be a month or more and I can’t wait that long!

The Electric Xtracycle: The S.E.E.P.’s Latest in Eco-Friendly Transportation!

Posted in Uncategorized on June 22, 2010 by theseep

I’ve had my xtracycle for a few years now and it’s served me well commuting around town and to French Hospital for work.  Now that we have Orion, we decided to go for xtracycle’s PeaPod promotion and got Laura their Radish model with the PeaPod child seat attachment.  Although the bike was quite a looker and very functional, the components left a little to be desired, so I upgraded the front crank from a single to triple chain ring, upgraded brakes levers and shifters, and rear derailleur to Shimano XT, swapped out a more practical handlebar, and put on the sweet seat from Laura’s old commuter.  While this worked well around town, the xtracycle setup and PeaPod made for a heavy bike and because of this, and time constraints, we weren’t using it as much as we wanted.  So, I overcame my biker’s guilt and we decided to electrify it through Jake at San Luis Rides.  We went with a high-end kit, including a 600W BMC V2 motor in the rear wheel, a 48V, a LiFePO4 48v 15AH Battery w/ charger, and the Cycle Analyst computer to monitor discharge status and mileage.  Along with Jake’s EV install, I also installed a 12V lighting system and some barrio fabuloso green ground effects, which required some research, making a bracket for the headlight and turn signals, and some wiring, then I wrapped all the wires up neatly with some spiral cable wrap and tucked the controller and 48v-12v inverter into a bag behind the seat.  After all was said and done, we now have a beautiful and efficient assisted mode of transportation for one of us with Orion and he loves it!  We get a top speed of around 27 mph (although we’re legally topped out at 20mph) and a range of 15-20 miles depending on how fast we’re cooking and how much we’re pedaling.  We’re definitely using the bike more for our around town errands and shopping with the motor than before.  Even though the xtracycle was great before, electrifying it has overcome the “energy of activation” that we needed to really ditch the car for most of our quick trips!

Here is the video we made for xtracycle as part of the “PeaPod Pilots” promotion they did:

Orion’s New Xtracycle PeaPod LT from Clint Slaughter on Vimeo.

DDT Use and Malaria: Review and Position Statement

Posted in Environmental Health, Uncategorized on March 31, 2010 by theseep

Author:  Clint Slaughter, M.D., Walden University MPH Student, 4/7/2009

Significance of Malaria

Malaria is a protozoan that is transmitted to humans through a carrier Anopheles mosquito and is the most important parasitic disease to affect humans (Braunwald, 1998, pg. 1180).  According to the World Health Organization’s (WHO) World Malaria Report 2008, there were approximately 247 million cases of malaria in 2006, 86% of them occurring in Africa, and leading to an estimated 881,000 deaths (2008).  Malaria rates peaked around 5 million cases per year in the 1930’s (Gates, 2009), and although significant progress has been made in the prevention and treatment of the disease, it is and will continue to be a major battleground for public health efforts.

There are four types of malaria that infect humans, Plasmodium vivax, Plasmodium ovale, Plasmodium malariae, and Plasmodium falciparum, with nearly all of the severe cases leading to death being caused by the falciparum subtype (Braunwald, pg.1180).   Frighteningly, the WHO estimates that 91% of the malaria cases in 2006 were due to this deadly strain of the disease (World malaria report, 2008).  The lifecycle of the parasite is important to understand so that effective interventions can be made to decrease transmission.  Humans are an essential part of this cycle, with malarial gametocytes being ingested by a mosquito during a blood meal from an infected human, which then form zygotes that then mature into infective sporozoites that migrate to the insect’s salivary glands.  These sporozoites are then injected into another human during another blood meal, starting the next phase of the lifecycle.  In human liver cells, the sporozoites develop into schizonts, which produce and release merozoites into the bloodstream.  Interestingly, in the ovale and vivax malarial subtypes, some of these organisms become dormant and stay in the liver cells, only to be reactivated sometimes years later with acute infection.  Once in the blood, the merozoites invade red blood cells where they further mature into hemoglobin-consuming trophozoites that then make more merozoites that are released when the red blood cell is spent and the cycle continues (Braunwald, pg 1180-81).
Active malaria infection causes a variety of symptoms including cyclic fevers, the lysis, or breaking of red blood cells that carry oxygen to the body, splenic enlargement and rupture, cerebral malaria with encephalopathy and coma, hypoglycemia, acidosis, kidney failure, and sometimes death (Braunwald, pg 1182-83).  Malaria has been a human health risk for so long, that mutations have arisen to protect certain populations from the disease, the most well-known being sickle-cell trait, where carriers have abnormal hemoglobin leading to early rupture of red blood cells that stops the intravascular reproductive cycle.  Glucose-6-phosphatase (G6PD) deficiency is an enzyme deficiency that acts similarly to sickle-cell trait (Braunwald, pg 663).  Also, certain populations in endemic malarial areas lack the Duffy blood-group antigen, which is required for P. vivax to infect cells (Braunwald, pg 1180).  Although the mutations can be beneficial in preventing severe malaria infections, they can also confer other health problems, since those homozygous for hemoglobin S, the sickle-cell trait, are very sensitive to low oxygenation or stress, lysing red blood cells even without a malarial infection, while those heterozygous for the trait with only one gene are protected from malaria with only minimal other effects (Braunwald, pg 648-50).

Intervention and control
The approach to intervention and control of malaria has already run the gamut, with governments, non-governmental organizations (NGOs), healthcare professionals and the like, utilizing the clinical intervention model, the public health intervention model, and the environmental stewardship model in attempting to decrease malaria transmission, morbidity and mortality (Moeller, 2005).  The clinical intervention model treats those who have already become ill, using chloroquine, mefloquine, or quinine, depending on the subtype and severity of the disease (Harrison’s, pg 1187).  Malaria is indeed treatable, but causes worse disease and has increased mortality However, because of the pervasiveness and severity of the disease, the public health intervention model must be used as well to educate those at risk with preventative practices.  Environmental stewardship is also paramount in fighting the disease to control the vectors to human disease.  There are many approaches to this model in regards to malaria, such as eliminating mosquito breeding areas (Sibbald, 2002) and the use of chemical agents such as DDT or peremptoriness to kill mosquito populations and mosquito larvae.  Some of these environmental approaches, such as the use of DDT, have demonstrated significant human health and environmental side effects that may outweigh the risks of the disease.  Bill Gates, who’s foundation has become a major player in the global fight against malaria, discussed some of these challenges in his TED talk this February, citing that treated nets plus indoor DDT spraying can cut deaths by over 50% (Gates, 2009).  Gates also addresses some of the challenges that we face in that not only can the malaria parasite itself develop resistance to drugs, but the vector mosquitoes also become resistant to insecticide.

Impact of DDT

Use of DDT
DDT, or 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane, was used extensively as an agricultural and domestic insecticide from the 1930’s to the 1970’s when it was banned in many countries, including the U.S..  It is a type of organochlorine pesticide that has a wide range of effectiveness against mosquitoes as well as many common agricultural insects such as potato beetles, the coddling moth, corn earworm, the cotton bollworm, and tobacco budworms (DDT: An Introduction, N.D.).  Because of its broad spectrum effectiveness and low cost, DDT saw wide use around the world beginning after WWII.  In the decades following, however, the agricultural application of the chemical caused widespread contamination of water, air, and soil, and was found to persist for decades in the environment (Toxicological Profile, 2002).

Similarly to other pesticides, DDT causes significant toxicity with large acute exposures or overdoses, causing neurologic impairment, headache, vomiting, tremors, and other effects (Third National Report, 2005), and after a few decades if use, it was blamed for many environmental phenomena as well.  In 1962, Rachel Carson, an environmental activist, wrote Silent Spring, a book documenting declines in bird populations, the presence of the chemical in fish, livestock, pets, and humans, and an association with cancer (Raloff, 2000).  After the publication of the book, public awareness and concern about the dangers of the widespread use of DDT became such that by the mid-1970’s, many countries such as the U.S. and much of Europe, had banned the use of the chemical.  The heavy use of DDT over just 40 years led to quantifiable changes in wildlife, as well as pressured insects such as mosquitoes, to begin demonstrating resistance to the chemical (Matambo, et al. 2007).  Encouragingly, since the ban, the bird populations affected have rebounded (Glausiusz, 2007).

DDT Controversy
DDT has remained in use in some areas and over the last few years has been in somewhat controversial use once again against mosquitoes in the fight against malaria.  Part of the reasoning behind this is the difference in usage, small-area spraying verses spraying entire agricultural areas, as well as an alarming rise in malaria cases in some areas since the ban, attributable to greater difficulty controlling mosquito populations without DDT (DDT: An Introduction, N.D.).  Over the decades since DDT was banned, more detailed information has been uncovered about its true effects on environmental and human health.  It seems that Carson was correct and even may have underestimated DDT’s effect on bird populations and hormonal influences on fish and amphibians (Raloff, 2000).  More research on the carcinogenic effects of the chemical show that the age of those exposed plays a role in risk for cancer, demonstrating an increased risk with exposures at younger ages (Cohn, Wolff, Cirillo, & Sholtz, 2007).  Continuing studies of the effects of DDT have also shown that rather than causing a large increase in cancer risk, it has similar estrogen-mimicking effects to many of our present-day chemical exposures such as Bisphenol-A and phthalates, as well as many modern, approved pesticides and fertilizers, increasing the risk of certain types of cancer with long-term and cumulative exposures (Third National Report, 2005).

Position Statement
Malaria is one of the most significant preventable and treatable diseases to continue to scourge humankind, so much so that it is one of the only environmental pressures through which we can actually see human evolution at work to protect ourselves against it in the form of sickle cell trait and G6PD deficiencies.  Malaria needs to be fought on many fronts:  education and prevention, eradicating the vector, the Anopheles mosquito, as well as medically treating the parasite itself once it has infected a human.  The more people infected, the more reservoir sources mosquitoes have to continue the lifecycle of malaria, the more mosquitoes, the more chance to infect more humans, and the cycle continues.
DDT is, thus far, the most effective chemical agent we have against mosquitoes and has been proven to decrease transmission of malaria when sprayed in homes (Gunasekaran, Sahu, Jambulingam, & Das, 2005), especially in conjunction with other prevention measures.  Despite this, DDT has been shown to cause significant environmental damage when used in large quantities for agricultural use, effecting avian and fish populations, pressuring mosquitoes to become resistant, as well as causing human health problems with moderate or high level exposures.
Although the decision to ban the use of DDT as an agricultural pesticide in the 1970’s was correct and should be upheld, the reasonable use of DDT to fight malaria continues to be a question of risk verses benefit.   At this juncture, the malaria epidemic in certain parts of the world, especially in Africa, does justify the use of DDT for this purpose specifically.    However, vigilance must be maintained and continued research is imperative to find more sustainable and less toxic methods to fight the disease, realizing that overuse of any chemical or method, be they pesticide or drug, will pressure these organisms to adapt and become resistant to our efforts.  DDT should be nothing more than a bridge to keep the malaria epidemic at bay as we look at improvements in mosquito control methods, through both environmental and chemical means, improvements in treatment of the disease itself, as well as continued efforts towards a vaccine.

Braunwald E, et. al., (ed.) (1998). Harrison’s Principles of Internal Medicine, 14th ed. New York, New York: McGraw Hill.

Centers for Disease Control (2005).  Third National Report on Human Exposure to Environmental Chemicals.  Retrieved on April 2, 2009 from: http://www.cdc.gov/exposurereport/pdf/results_08.pdf

Cohn, B., Wolff, M., Cirillo, P., & Sholtz, R. (2007). DDT and breast cancer in young women: New data on the significance of age at exposure. Environmental Health Perspectives, 115(10), 1406–1414. Retrieved on April 2, 2009 from Walden Library Academic Search Premier database.

Duke University (n.d.).  DDT:  An Introduction. Retrieved on April 2, 2009 from: http://www.chem.duke.edu/~jds/cruise_chem/pest/pest1.html

Gates, W. (2009).  TED Talks Bill Gates:  How I’m trying to change the world now (Video).  Retrieved on April 2, 2009 from: http://www.ted.com/index.php/talks/bill_gates_unplugged.html

Glausiusz, J. (2007, November). Can a maligned pesticide save lives?. Discover, 28(11), 34-36. Retrieved April 2, 2009, from Academic Search Premier database.

Gunasekaran, K., Sahu, S., Jambulingam, P., & Das, P. (2005, February). DDT indoor residual spray, still an effective tool to control Anopheles fluviatilis-transmitted Plasmodium falciparum malaria in India. Tropical Medicine & International Health, 10(2), 160-168. Retrieved April 2, 2009

Lewis, K. (2008, November 4). DDT stalemate stymies malaria control initiative. CMAJ: Canadian Medical Association Journal, 179(10), 999-1000. Retrieved April 2, 2009, from Academic Search Premier database.

Matambo, T., Abdalla, H., Brooke, B., Koekemoer, L., Mnzava, A., Hunt, R., et al. (2007). Insecticide resistance in the malarial mosquito Anopheles arabiensis and association with the kdr mutation. Medical & Veterinary Entomology, 21(1), 97-102. Retrieved April 2, 2009, from Academic Search Premier database.

Moeller, D. W. (2005). Environmental Health (third ed.). Cambridge, MA: Harvard University Press.

Raloff, J. (2000, July). The Case for DDT. Science News, 158(1), 12. Retrieved April 2, 2009, from Academic Search Premier database.

Salazar-García, F., Gallardo-Díaz, E., Cerón-Mireles, P., & Borja-Aburto, V. (2004). Reproductive Effects of Occupational DDT Exposure among Male Malaria Control Workers, Environmental Health Perspectives, 112 (5), 542-547.

Sibbald, B. (2002). DDT use finally eliminated in North America. CMAJ: Canadian Medical Association Journal, 166(10), 1322. Retrieved April 2, 2009, from Academic Search Premier database.

World Health Organization (2008).  World malaria report 2008.  Retrieved on April 2, 2009 from:  http://www.who.int/malaria/wmr2008/

U.S. Department of Health and Human Services (2002).  Toxicological Profile for DDT, DDE, and DDD.  Retrieved on April 2, 2009 from:  http://www.atsdr.cdc.gov/toxprofiles/tp35.html

A Brief Essay on The History and Dangers of Trans Fats.

Posted in Environmental Health, Uncategorized on March 28, 2010 by theseep
Author: Clint Slaughter, M.D., March 19, 2009

Rather than an infectious or outright chemical additive to food, our industrial food process has developed many ways to modify what we eat into other forms with occasionally unanticipated and disastrous results. The introduction of chemically modified trans-fats, formerly known as “partiallly hydrogenated” fats, into our diets over the course of the 20th century is one example of industrial food manipulation gone wrong. Vegetable oil comes in many natural and unnatural forms, the four main types in our diet being saturated fat, monounsaturated fat, polyunsaturated fat, and trans fats, all of which affect the body slightly differently (Fats 101, 2009). Saturated fats and trans fats are considered the “bad fats”, which have been found to increase Low Density Lipoproteins (LDLs), or “bad cholesterol”, when consumed regularly (de Roos, Bots, Katan, 2001), saturated fats also being more Trans Fat Fryercalorically dense than unsaturated fats. Since 1990, however, many studies have shown that the artificially modified trans fats have many more deleterious health effects, significantly contributing to vascular and coronary artery disease in various ways (Mozaffarian, Katan, Ascherio, Stampfer, Willett, 2006).

Partially hydrogenated oils were first introduced to the American Public in the form of Crisco in 1911 (A History of Trans Fats, 2008). A chemical reaction causes the natural cis, or same-side bond in a fatty acid chain to be converted to a trans, or opposite side bond. This actually straightens the molecule so that it becomes a more solid substance which allows for longer shelf life, longer use in fryers, and forms solid shortenings and margerine from liquid oil. Since the 1990’s, more and more studies have demonstrated that trans fats have many more health effects than natural fats, even the more caloric saturated fats. An excellent review of the current literature was published in the New England Journal of Medicine in 2006, discussed these many health issues, including elevated LDLs, and triglycerides, decreased High Density Lipoproteins (HDLs), or “good cholesterol”, increased systemic inflammation, and impaired endothelial cell dysfunction, all of which contribute to atherosclerosis, vascular disease, and coronary artery disease (Mozaffarian, et al, 2006). Another study looked at the effects of trans fats on flow-mediated vasodilation (FMD), another risk marker for vascular disease, and found that in comparison with saturated fats, trans fats decreased normal FMD, presumably further increasing cardiac risk (de Roos, et al, 2001).

Cardiovascular disease is the number one cause of death in the United States, leading to nearly 8 million heart attacks a year and 6.5 million strokes (Cardiovascular Disease Statistics, 2009). The American Heart Association notes that in 2005, this translates to 864,480 deaths, or 35.3% of U.S. deaths, in comparison to 559,312 deaths from cancer, and 117,809 deaths from accidents. Unfortunately, trans fats have become a part of every American’s diet through margarine, fried foods, trans fats added to foods, it is ubiquitous in our industrial food supply, effecting all of us. As cardiovascular disease has increased over the last century, the addition of trans fats into the American diet has undoubedtly been a factor in the rise of our number one killer. As a testament to the public health system, the healthcare system, and the scientific community, over the last few years, trans fats have become a source of national attention. Through grass-roots activism and public health efforts, trans fats are being discouraged and even outlawed in New York City in 2006 and in California in 2007. More education is needed for consumers to be able to distinguish between types of fats and look for trans fats in labels where they are still available.


American Heart Association (2008). A History of Trans Fats. Retrieved on March 19, 2009 from: http://www.americanheart.org/presenter.jhtml?identifier=3048193

American Heart Association (2009). Cardiovascular Disease Statistics. Retrieved on March 19, 2009 from: http://www.americanheart.org/presenter.jhtml?identifier=4478

American Heart Association (2009). Fats 101. Retrieved on March 19, 2009 from: http://www.americanheart.org/presenter.jhtml?identifier=3045789

American Heart Association (2009). Trans Fats. Retrieved on March 19, 2009 from: http://www.americanheart.org/presenter.jhtml?identifier=3045792

de Roos, M., Bots, L., Katan, M. (2001). Replacement of Dietary Saturated Fatty Acids by Trans Fatty Acids Lowers Serum HDL Cholesterol and Impairs Endothelial Function in Healthy Men and Women
Arteriosclerosis, Thrombosis, and Vascular Biology. 21: 1233 – 1237. Retrieved on March 19, 2009 from: http://atvb.ahajournals.org/cgi/content/full/21/7/1233

Mozaffarian, D., Katan, M., Ascherio, A., Stampfer, M., Willett W. (2006). Trans fatty acids and cardiovascular disease. New England Journal of Medicine. 354:15. 1601-13. Retrieved on March 19, 2009 from http://content.nejm.org/cgi/content/full/354/15/1601?ijkey=/Ulbtkh3itKkQ&keytype=ref&siteid=nejm

The S.E.E.P. is Back in School – Master’s of Public Health from Walden University

Posted in Uncategorized on March 11, 2010 by theseep

I apologize to any regular readers for the paucity of posts over the past year, I am now just over halfway through a Master’s of Public Health Degree from Walden University online while continuing to work as an ER physician and helping with our now 8 month old son Orion.  My wife Laura is back in school as well for a Master’s of Nursing Education, so we’ve been very busy while enjoying our new family at home.

I’m concentrating on environmental health and will begin posting relevant essays from classes with citations, shifting some of the writing on theseep.com from my generally well-informed, standard rants to articles with reliable sources and citations so that readers can look further into issues and see the basic research behind the rants.

Orion’s Xtracycle and Peapod Commercial

Posted in alternative fuel, clean energy, conservation, ethical consumerism, global warming, sustainability, transportation on February 13, 2010 by theseep

I’ve thoroughly enjoyed my Xtracycle over the last 3 years and it was time to figure out a mode of eco-friendly transport for Orion, so we opted to upgrade Laura’s commuter to an Xtracycle Radish model with the Peapod child carrier kit. They had a promotion that required us to make a video, submit a testimonial and some photos for almost $400 off the package!

At 7 months Orion is almost ready to take his first trip to Farmer’s Market on his new bike limousine! Of course, we’re still using biodiesel and vegetable oil for our vehicle transport, but cycling is still preferred when we can (you really pay attention to how much fuel you use when you make it yourself!).