Johns Hopkins University President calls for increased funding and support for young scientists

In the most recent issue of PNAS, the president of my alma mater, Ronald J. Donalds, discusses the disturbing trend of decreased funding for young scientists saying, “The departure of young scientists from the academic biomedical workforce in turn poses grave risks for the future of science.”

Fig 1 from article: Percent of NIH R01 principal investigators and medical school faculty by age (1980 in pale and 2010 in bold).

The R01 grant from the National Institutes of Health (NIH) is one of the largest and most important grants for scientists to independently fund and maintain their careers. Donalds says that the number of scientists 36 or younger who received an R01 dropped from 18% in 1983 to 3% in 2010.

In the article he addresses several theories for why young scientists aren’t receiving grants, including inherent bias in the grant process towards more established scientists, the financial hardship placed on institutions in supporting faculty, and the protracted postdoctoral training period which increases the average age a scientist obtains a faculty position.

He goes on to address each point. In regards to the long training periods he makes several suggestions. As it is well known and recorded that there are far more postdoctoral researchers than available faculty positions, Donalds calls for better career training. “To provide a true foundation of support for early-stage scientists, we will need to construct a pathway to a career in the biomedical sciences that is sustainable, humane and fair.” One solution Donalds offers are more staff scientist positions at core facilities in universities and research institutions.

Donalds also cites the need for “weaning our biomedical workforce away from an overreliance on postdoctoral researchers.” A decade-old report by the National Academy of Sciences suggested imposing a 5-year limit on funding for postdocs, which Donalds suggests should be revisited. He also suggests increased K99/R00 grants, which provide funding for postdoc training as well as establishing their own independent career. Finally he says there is a need for “demystifying the R01” as the most important factor for obtaining and retaining faculty.

Antibacterial everything: should we be putting triclosan in consumer products?

Triclosan is an antibacterial and antifungal agent that has been used in the hospital setting since the 1970s. In the last decades, triclosan has increasingly been added to household products including hand soaps and wipes, body washes, and toothpastes. It is now even found in some products that consumers may not be aware of, including toys. The safety and efficacy of triclosan has been debated for years, but this last year saw major milestones. In 2014, Minnesota became the first state in U.S. to ban triclosan in soaps and several major companies, including Johnson & Johnson announced they would phase out triclosan from their products. In a 2010 consumer report, the FDA said that there was no evidence that triclosan was hazardous to humans, yet a 2013 consumer report cited an FDA microbiologist, “the risks associated with long-term, daily use of antibacterial soaps may outweigh the benefits (1,2)”. The FDA is currently evaluating its regulations on triclosan and is set to make a final decision in 2016.

The controversy surrounding triclosan is really on three levels: what the compound does to bacteria, possibly creating antibiotic resistance, what it does to humans when they ingest or absorb triclosan through the skin, and finally, what it does to the environment. The latest research on each front is presented here.

Colgate Total

1. Effect on microbes:

The microbes that could be affected by triclosan-containing products include the bacteria on your hands, in your household or environment, and those inside of you, which make up the microflora.

The late 1990s, early 2000s saw a drastic increase in the number of publications on antibiotic-resistance and triclosan. While there are discrepancies in the literature, the field is generally in agreement that triclosan use at the levels found in consumer products selects for and promotes triclosan resistant bacteria in the gut or on skin, including Salmonella enterica, E. coli and the MRSA-causing opportunistic bacteria, Staphylococcus aureus (7).

The FDA concluded in 1997 that triclosan in toothpaste was safe and effective at preventing gingivitis (1). However, questions have since arisen as toothpaste accounts for the greatest amount of ingested triclosan in humans. Many studies support the claim for reduced gingivitis and show that dental plaque bacteria do not become resistant to the triclosan even with nearly two decades use in toothpaste (3-6). But beyond fighting gingivitis, the FDA has not found any other health benefits of using triclosan-containing products, reporting that there was no “evidence that triclosan in antibacterial soaps and body washes provides any benefit over washing with regular soap and water (1).”

Last year, Syed et al. reported that triclosan was present in the nasal secretions of 50% of healthy adults. Triclosan levels were positively correlated with colonization by S. aureus, which is a risk factor for other infections. Rats given triclosan were more likely to have nasal infections by S. aureus. Intriguingly, the authors concluded that triclosan appears to induce changes in the bacteria that increase binding to surfaces such as host cells (8). 

2. Effect on human physiology:

Triclosan is absorbed through the skin with topical use and through the GI tract and oral mucosa when ingested. Triclosan is detectable in most people, through serum, milk, and urine (9, 10). Triclosan binds the human estrogen receptor, though weakly (11) and it is thought that triclosan may act an endocrine disruptor, causing hormonal changes that could lead to cancer. Several studies have linked triclosan to thyroid and liver dysfunction in mice or rats (12, 13). However the concentrations used were several orders of magnitude higher than to what humans are exposed. Epidemiological studies on human populations have not provided evidence that triclosan poses a health risk through endocrine disruption (14). However a recent study looked at the effects of low levels of triclosan (based on those found in humans) on mammary gland development in rats. While there was no effect on rats that have never given birth, those that had given birth experienced changes to their mammary glands, with decreased lactation and changes in gene expression (15). Therefore, further testing is required to understand the real threat posed to humans by long-term triclosan exposure.

3. Environmental effects:

Of note, the EPA and FDA have begun working together in evaluating the risks of triclosan. While most triclosan is removed at wastewater treatment facilities, significant amounts still end up in water sources and have been found in fish (16-18). Recent studies in natural water sources near urban populations, where triclosan levels are the highest, showed a correlation between triclosan levels and resistance of bacteria to triclosan Artificial stream experiments, where experimental factors are more controlled, backed up the findings and found that triclosan exposure was toxic to algae and led to a dramatic increase in cyanobacteria, indicating large changes in the stream ecosystem (16). Other studies found changes in the populations of phytoplankton, a key player in water ecosystems, including decreased photosynthesis with triclosan exposure (17, 18).

Though more studies are needed to understand the full risks posed by low level exposure to triclosan, it is likely that public opinion will go the way of bisphenol A. As for now the safest bet is to use regular soap for hand washing and triclosan-containing toothpastes only if recommended by your dentist.

References:

1. FDA Consumer Health Information (2010). Triclosan: What Consumers Should Know

 <http://www.fda.gov/forconsumers/consumerupdates/ucm205999.htm>. Accessed Jan 1, 2015.

 2. FDA For Consumers. (2013). FDA Taking Closer Look at 'Antibacterial' Soap. < http://www.fda.gov/forconsumers/consumerupdates/ucm378393.htm>. Accessed Jan 1 2015.

 3. Haraszthy, VI., et al. (2014). Community-level assessment of dental plaque bacteria susceptibility to triclosan over 19 years. BMC Oral Health. 14:6.

 4. Cullinan, M.P., et al. (2013). No evidence of triclosan-resistant bacteria following long-term use of triclosan-containing toothpaste. J Periodontal Res. doi:10.1111/jre.12098.

 5. Niederman, R. (2005). Triclosan-containing toothpastes reduce plaque and gingivitis. Evid Based Dent. 6:33.

 6. Davies, R.M., et al. (2004). The effectiveness of a toothpaste containing triclosan and polyvinyl-methyl ether maleic acid copolymer in improving plaque control and gingival health: a systematic review. J Clin Periodontol. 31:1029–1033.

 7. Yazdankhah, S.P., et al. (2005). Triclosan and Antimicrobial Resistance in Bacteria:

An Overview. Microb Drug Resis. 12: 83-91.

 8. Syed, A.K. et al. (2014). Triclosan Promotes Staphylococcus aureus Nasal Colonization. mBio. 15: e01015-13.

 9. Calafat, A.M., et al. (2008). Urinary concentrations of triclosan in the U.S. population: 2003–2004. Environ. Health Perspect. 116:303–307.

 10 – Allmyr, M. et al.. (2006). Triclosan in plasma and milk from Swedish nursing mothers and their exposure via personal care products. Sci. Total Environ. 372:87–93.

 11. Ahn, K.C., et al. (2008). In vitro biologic activities of the antimicrobials triclocarban, its analogs, and triclosan in bioassay screens: receptor-based bioassay screens. Environ. Health Perspect. 116:1203–1210.

 12. Yueh, M.F., et al. (2014). The commonly used antimicrobial additive triclosan is a liver tumor promoter. PNAS. 111: 17200–17205.

13. Halden, R. (2014). On the Need and Speed of Regulating Triclosan and Triclocarban in the United States. Environ. Sci. Technol. 48: 3603-3611. 

 14. Witorsch, R. (2014). Critical analysis of endocrine disruptive activity of triclosan and its relevance to human exposure through the use of personal care products. Crit Rev Toxicol. 44: 535–555.

 15. Manservisi F., et al. (2014). Effect of maternal exposure to endocrine disrupting chemicals on reproduction and mammary gland development in female sprague-dawley rats. Reprod Tox. http://dx.doi.org/10.1016/j.reprotox.2014.12.013.

 16. Drury, B., et al. (2013). Triclosan exposure increases triclosan resistance and influences taxonomic composition of benthic bacterial communities. Environ. Sci. Technol. 47:8923–8930.

 17. Ricarta, M., et al. (2010). Triclosan persistence through wastewater treatment plants and its potential toxic effects on river biofilms. Aquatic Tox. http://dx.doi.org/10.1016/j.aquatox.2010.08.010.

18. Pomati, F. and L. Nizzetto. (2013). Assessing triclosan-induced ecological and trans-generational effects in natural phytoplankton communities: a trait-based field method. Ecotoxicology. 22: 779-94.