ABSTRACT
BACKGROUND: Per- and polyfluoroalkyl substances (PFAS) are environmental contaminants that are potentially harmful to health. We examined if rates of selected cancers and causes of deaths were elevated in three Australian communities with local environmental contamination caused by firefighting foams containing PFAS. The affected Australian communities were Katherine in Northern Territory, Oakey in Queensland and Williamtown in New South Wales. METHODS: All residents identified in the Medicare Enrolment File (1983-2019)-a consumer directory for Australia's universal healthcare-who ever lived in an exposure area (Katherine, Oakey and Williamtown), and a sample of those who ever lived in selected comparison areas, were linked to the Australian Cancer Database (1982-2017) and National Death Index (1980-2019). We estimated standardised incidence ratios (SIRs) for 23 cancer outcomes, four causes of death and three control outcomes, adjusting for sex, age and calendar time of diagnosis. FINDINGS: We observed higher rates of prostate cancer (SIR=1·76, 95 % confidence interval (CI) 1·36-2·24) in Katherine; laryngeal cancer (SIR=2·71, 95 % CI 1·30-4·98), kidney cancer (SIR=1·82, 95 % CI 1·04-2·96) and coronary heart disease (CHD) mortality (SIR=1·81, 95 % CI 1·46-2·33) in Oakey; and lung cancer (SIR=1·83, 95 % CI 1·39-2·38) and CHD mortality (SIR=1·22, 95 % CI 1·01-1·47) in Williamtown. We also saw elevated SIRs for control outcomes. SIRs for all other outcomes and overall cancer were similar across exposure and comparison areas. INTERPRETATION: There was limited evidence to support an association between living in a PFAS exposure area and risks of cancers or cause-specific deaths.
Subject(s)
Fluorocarbons , Kidney Neoplasms , Neoplasms , Prostatic Neoplasms , Male , Humans , Aged , Cohort Studies , Australia/epidemiology , Semantic Web , National Health Programs , Incidence , Prostatic Neoplasms/complications , Kidney Neoplasms/complicationsABSTRACT
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ABSTRACT
Cumulative cultural evolution occurs when social traditions accumulate improvements over time. In humans cumulative cultural evolution is thought to depend on a unique suite of cognitive abilities, including teaching, language and imitation. Tool-making New Caledonian crows show some hallmarks of cumulative culture; but this claim is contentious, in part because these birds do not appear to imitate. One alternative hypothesis is that crows' tool designs could be culturally transmitted through a process of mental template matching. That is, individuals could use or observe conspecifics' tools, form a mental template of a particular tool design, and then reproduce this in their own manufacture - a process analogous to birdsong learning. Here, we provide the first evidence supporting this hypothesis, by demonstrating that New Caledonian crows have the cognitive capacity for mental template matching. Using a novel manufacture paradigm, crows were first trained to drop paper into a vending machine to retrieve rewards. They later learnt that only items of a particular size (large or small templates) were rewarded. At test, despite being rewarded at random, and with no physical templates present, crows manufactured items that were more similar in size to previously rewarded, than unrewarded, templates. Our results provide the first evidence that this cognitive ability may underpin the transmission of New Caledonian crows' natural tool designs.
Subject(s)
Crows/physiology , Memory, Short-Term/physiology , Tool Use Behavior/physiology , Animals , Biological Evolution , Cognition/physiology , Female , Food Dispensers, Automatic , Imitative Behavior/physiology , Intelligence Tests , Male , Reward , Statistics, NonparametricABSTRACT
Advances in cannabis research have paralleled developments in opioid pharmacology whereby a psychoactive plant extract has elucidated novel endogenous signalling systems with therapeutic significance. Cannabinoids (CBs) are chemical compounds derived from cannabis. The major psychotropic CB delta-9-tetrahydrocannabinol (Delta(9)-THC) was isolated in 1964 and the first CB receptor (CB(1)R) was cloned in 1990. CB signalling occurs via G-protein-coupled receptors distributed throughout the body. Endocannabinoids are derivatives of arachidonic acid that function in diverse physiological systems. Neuronal CB(1)Rs modulate synaptic transmission and mediate psychoactivity. Immune-cell CB(2) receptors (CB(2)R) may down-regulate neuroinflammation and influence cyclooxygenase-dependent pathways. Animal models demonstrate that CBRs play a fundamental role in peripheral, spinal, and supraspinal nociception and that CBs are effective analgesics. Clinical trials of CBs in multiple sclerosis have suggested a benefit in neuropathic pain. However, human studies of CB-mediated analgesia have been limited by study size, heterogeneous patient populations, and subjective outcome measures. Furthermore, CBs have variable pharmacokinetics and can manifest psychotropism. They are currently licensed as antiemetics in chemotherapy and can be prescribed on a named-patient basis for neuropathic pain. Future selective peripheral CB(1)R and CB(2)R agonists will minimize central psychoactivity and may synergize opioid anti-nociception. This review discusses the basic science and clinical aspects of CB pharmacology with a focus on pain medicine.